--- _id: '21' abstract: - lang: eng text: Parvalbumin-positive (PV+) GABAergic interneurons in hippocampal microcircuits are thought to play a key role in several higher network functions, such as feedforward and feedback inhibition, network oscillations, and pattern separation. Fast lateral inhibition mediated by GABAergic interneurons may implement a winner-takes-all mechanism in the hippocampal input layer. However, it is not clear whether the functional connectivity rules of granule cells (GCs) and interneurons in the dentate gyrus are consistent with such a mechanism. Using simultaneous patch-clamp recordings from up to seven GCs and up to four PV+ interneurons in the dentate gyrus, we find that connectivity is structured in space, synapse-specific, and enriched in specific disynaptic motifs. In contrast to the neocortex, lateral inhibition in the dentate gyrus (in which a GC inhibits neighboring GCs via a PV+ interneuron) is ~ 10-times more abundant than recurrent inhibition (in which a GC inhibits itself). Thus, unique connectivity rules may enable the dentate gyrus to perform specific higher-order computations acknowledgement: This project received funding from the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement No 692692) and the Fond zur Förderung der Wissenschaftlichen Forschung (Z 312-B27, Wittgenstein award), both to P.J.. article_number: '4605' article_processing_charge: No article_type: original author: - first_name: 'Claudia ' full_name: 'Espinoza Martinez, Claudia ' id: 31FFEE2E-F248-11E8-B48F-1D18A9856A87 last_name: Espinoza Martinez orcid: 0000-0003-4710-2082 - first_name: José full_name: Guzmán, José id: 30CC5506-F248-11E8-B48F-1D18A9856A87 last_name: Guzmán orcid: 0000-0003-2209-5242 - first_name: Xiaomin full_name: Zhang, Xiaomin id: 423EC9C2-F248-11E8-B48F-1D18A9856A87 last_name: Zhang - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Espinoza Martinez C, Guzmán J, Zhang X, Jonas PM. Parvalbumin+ interneurons obey unique connectivity rules and establish a powerful lateral-inhibition microcircuit in dentate gyrus. Nature Communications. 2018;9(1). doi:10.1038/s41467-018-06899-3 apa: Espinoza Martinez, C., Guzmán, J., Zhang, X., & Jonas, P. M. (2018). Parvalbumin+ interneurons obey unique connectivity rules and establish a powerful lateral-inhibition microcircuit in dentate gyrus. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/s41467-018-06899-3 chicago: Espinoza Martinez, Claudia , José Guzmán, Xiaomin Zhang, and Peter M Jonas. “Parvalbumin+ Interneurons Obey Unique Connectivity Rules and Establish a Powerful Lateral-Inhibition Microcircuit in Dentate Gyrus.” Nature Communications. Nature Publishing Group, 2018. https://doi.org/10.1038/s41467-018-06899-3. ieee: C. Espinoza Martinez, J. Guzmán, X. Zhang, and P. M. Jonas, “Parvalbumin+ interneurons obey unique connectivity rules and establish a powerful lateral-inhibition microcircuit in dentate gyrus,” Nature Communications, vol. 9, no. 1. Nature Publishing Group, 2018. ista: Espinoza Martinez C, Guzmán J, Zhang X, Jonas PM. 2018. Parvalbumin+ interneurons obey unique connectivity rules and establish a powerful lateral-inhibition microcircuit in dentate gyrus. Nature Communications. 9(1), 4605. mla: Espinoza Martinez, Claudia, et al. “Parvalbumin+ Interneurons Obey Unique Connectivity Rules and Establish a Powerful Lateral-Inhibition Microcircuit in Dentate Gyrus.” Nature Communications, vol. 9, no. 1, 4605, Nature Publishing Group, 2018, doi:10.1038/s41467-018-06899-3. short: C. Espinoza Martinez, J. Guzmán, X. Zhang, P.M. Jonas, Nature Communications 9 (2018). date_created: 2018-12-11T11:44:12Z date_published: 2018-11-02T00:00:00Z date_updated: 2024-03-27T23:30:31Z day: '02' ddc: - '570' department: - _id: PeJo doi: 10.1038/s41467-018-06899-3 ec_funded: 1 external_id: isi: - '000449069700009' file: - access_level: open_access checksum: 9fe2a63bd95a5067d896c087d07998f3 content_type: application/pdf creator: dernst date_created: 2018-12-17T15:41:57Z date_updated: 2020-07-14T12:45:28Z file_id: '5715' file_name: 2018_NatureComm_Espinoza.pdf file_size: 4651930 relation: main_file file_date_updated: 2020-07-14T12:45:28Z has_accepted_license: '1' intvolume: ' 9' isi: 1 issue: '1' language: - iso: eng license: https://creativecommons.org/licenses/by/4.0/ month: '11' oa: 1 oa_version: Published Version project: - _id: 25B7EB9E-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '692692' name: Biophysics and circuit function of a giant cortical glumatergic synapse - _id: 25C5A090-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Z00312 name: The Wittgenstein Prize publication: Nature Communications publication_status: published publisher: Nature Publishing Group publist_id: '8034' quality_controlled: '1' related_material: link: - description: News on IST Homepage relation: press_release url: https://ist.ac.at/en/news/lateral-inhibition-keeps-similar-memories-apart/ record: - id: '6363' relation: dissertation_contains status: public scopus_import: '1' status: public title: Parvalbumin+ interneurons obey unique connectivity rules and establish a powerful lateral-inhibition microcircuit in dentate gyrus tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 9 year: '2018' ... --- _id: '630' abstract: - lang: eng text: 'Background: Standards have become available to share semantically encoded vital parameters from medical devices, as required for example by personal healthcare records. Standardised sharing of biosignal data largely remains open. Objectives: The goal of this work is to explore available biosignal file format and data exchange standards and profiles, and to conceptualise end-To-end solutions. Methods: The authors reviewed and discussed available biosignal file format standards with other members of international standards development organisations (SDOs). Results: A raw concept for standards based acquisition, storage, archiving and sharing of biosignals was developed. The GDF format may serve for storing biosignals. Signals can then be shared using FHIR resources and may be stored on FHIR servers or in DICOM archives, with DICOM waveforms as one possible format. Conclusion: Currently a group of international SDOs (e.g. HL7, IHE, DICOM, IEEE) is engaged in intensive discussions. This discussion extends existing work that already was adopted by large implementer communities. The concept presented here only reports the current status of the discussion in Austria. The discussion will continue internationally, with results to be expected over the coming years.' alternative_title: - Studies in Health Technology and Informatics author: - first_name: Stefan full_name: Sauermann, Stefan last_name: Sauermann - first_name: Veronika full_name: David, Veronika last_name: David - first_name: Alois full_name: Schlögl, Alois id: 45BF87EE-F248-11E8-B48F-1D18A9856A87 last_name: Schlögl orcid: 0000-0002-5621-8100 - first_name: Reinhard full_name: Egelkraut, Reinhard last_name: Egelkraut - first_name: Matthias full_name: Frohner, Matthias last_name: Frohner - first_name: Birgit full_name: Pohn, Birgit last_name: Pohn - first_name: Philipp full_name: Urbauer, Philipp last_name: Urbauer - first_name: Alexander full_name: Mense, Alexander last_name: Mense citation: ama: 'Sauermann S, David V, Schlögl A, et al. Biosignals standards and FHIR: The way to go. In: Vol 236. IOS Press; 2017:356-362. doi:10.3233/978-1-61499-759-7-356' apa: 'Sauermann, S., David, V., Schlögl, A., Egelkraut, R., Frohner, M., Pohn, B., … Mense, A. (2017). Biosignals standards and FHIR: The way to go (Vol. 236, pp. 356–362). Presented at the eHealth: Health Informatics Meets eHealth, Vienna, Austria: IOS Press. https://doi.org/10.3233/978-1-61499-759-7-356' chicago: 'Sauermann, Stefan, Veronika David, Alois Schlögl, Reinhard Egelkraut, Matthias Frohner, Birgit Pohn, Philipp Urbauer, and Alexander Mense. “Biosignals Standards and FHIR: The Way to Go,” 236:356–62. IOS Press, 2017. https://doi.org/10.3233/978-1-61499-759-7-356.' ieee: 'S. Sauermann et al., “Biosignals standards and FHIR: The way to go,” presented at the eHealth: Health Informatics Meets eHealth, Vienna, Austria, 2017, vol. 236, pp. 356–362.' ista: 'Sauermann S, David V, Schlögl A, Egelkraut R, Frohner M, Pohn B, Urbauer P, Mense A. 2017. Biosignals standards and FHIR: The way to go. eHealth: Health Informatics Meets eHealth, Studies in Health Technology and Informatics, vol. 236, 356–362.' mla: 'Sauermann, Stefan, et al. Biosignals Standards and FHIR: The Way to Go. Vol. 236, IOS Press, 2017, pp. 356–62, doi:10.3233/978-1-61499-759-7-356.' short: S. Sauermann, V. David, A. Schlögl, R. Egelkraut, M. Frohner, B. Pohn, P. Urbauer, A. Mense, in:, IOS Press, 2017, pp. 356–362. conference: end_date: 2017-05-24 location: Vienna, Austria name: 'eHealth: Health Informatics Meets eHealth' start_date: 2017-05-23 date_created: 2018-12-11T11:47:36Z date_published: 2017-01-01T00:00:00Z date_updated: 2021-01-12T08:06:59Z day: '01' ddc: - '005' department: - _id: ScienComp - _id: PeJo doi: 10.3233/978-1-61499-759-7-356 file: - access_level: open_access checksum: 1254dcc5b04a996d97fad9a726b42727 content_type: application/pdf creator: system date_created: 2018-12-12T10:11:56Z date_updated: 2020-07-14T12:47:27Z file_id: '4913' file_name: IST-2017-906-v1+1_SHTI236-0356.pdf file_size: 443635 relation: main_file file_date_updated: 2020-07-14T12:47:27Z has_accepted_license: '1' intvolume: ' 236' language: - iso: eng license: https://creativecommons.org/licenses/by-nc/4.0/ month: '01' oa: 1 oa_version: Published Version page: 356 - 362 publication_identifier: isbn: - 978-161499758-0 publication_status: published publisher: IOS Press publist_id: '7164' pubrep_id: '906' quality_controlled: '1' scopus_import: 1 status: public title: 'Biosignals standards and FHIR: The way to go' tmp: image: /images/cc_by_nc.png legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) short: CC BY-NC (4.0) type: conference user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 236 year: '2017' ... --- _id: '706' abstract: - lang: eng text: A hippocampal mossy fiber synapse has a complex structure and is implicated in learning and memory. In this synapse, the mossy fiber boutons attach to the dendritic shaft by puncta adherentia junctions and wrap around a multiply-branched spine, forming synaptic junctions. We have recently shown using transmission electron microscopy, immunoelectron microscopy and serial block face-scanning electron microscopy that atypical puncta adherentia junctions are formed in the afadin-deficient mossy fiber synapse and that the complexity of postsynaptic spines and mossy fiber boutons, the number of spine heads, the area of postsynaptic densities and the density of synaptic vesicles docked to active zones are decreased in the afadin-deficient synapse. We investigated here the roles of afadin in the functional differentiations of the mossy fiber synapse using the afadin-deficient mice. The electrophysiological studies showed that both the release probability of glutamate and the postsynaptic responsiveness to glutamate were markedly reduced, but not completely lost, in the afadin-deficient mossy fiber synapse, whereas neither long-term potentiation nor long-term depression was affected. These results indicate that afadin plays roles in the functional differentiations of the presynapse and the postsynapse of the hippocampal mossy fiber synapse. author: - first_name: Xiaoqi full_name: Geng, Xiaoqi id: 3395256A-F248-11E8-B48F-1D18A9856A87 last_name: Geng - first_name: Tomohiko full_name: Maruo, Tomohiko last_name: Maruo - first_name: Kenji full_name: Mandai, Kenji last_name: Mandai - first_name: Irwan full_name: Supriyanto, Irwan last_name: Supriyanto - first_name: Muneaki full_name: Miyata, Muneaki last_name: Miyata - first_name: Shotaro full_name: Sakakibara, Shotaro last_name: Sakakibara - first_name: Akira full_name: Mizoguchi, Akira last_name: Mizoguchi - first_name: Yoshimi full_name: Takai, Yoshimi last_name: Takai - first_name: Masahiro full_name: Mori, Masahiro last_name: Mori citation: ama: Geng X, Maruo T, Mandai K, et al. Roles of afadin in functional differentiations of hippocampal mossy fiber synapse. Genes to Cells. 2017;22(8):715-722. doi:10.1111/gtc.12508 apa: Geng, X., Maruo, T., Mandai, K., Supriyanto, I., Miyata, M., Sakakibara, S., … Mori, M. (2017). Roles of afadin in functional differentiations of hippocampal mossy fiber synapse. Genes to Cells. Wiley-Blackwell. https://doi.org/10.1111/gtc.12508 chicago: Geng, Xiaoqi, Tomohiko Maruo, Kenji Mandai, Irwan Supriyanto, Muneaki Miyata, Shotaro Sakakibara, Akira Mizoguchi, Yoshimi Takai, and Masahiro Mori. “Roles of Afadin in Functional Differentiations of Hippocampal Mossy Fiber Synapse.” Genes to Cells. Wiley-Blackwell, 2017. https://doi.org/10.1111/gtc.12508. ieee: X. Geng et al., “Roles of afadin in functional differentiations of hippocampal mossy fiber synapse,” Genes to Cells, vol. 22, no. 8. Wiley-Blackwell, pp. 715–722, 2017. ista: Geng X, Maruo T, Mandai K, Supriyanto I, Miyata M, Sakakibara S, Mizoguchi A, Takai Y, Mori M. 2017. Roles of afadin in functional differentiations of hippocampal mossy fiber synapse. Genes to Cells. 22(8), 715–722. mla: Geng, Xiaoqi, et al. “Roles of Afadin in Functional Differentiations of Hippocampal Mossy Fiber Synapse.” Genes to Cells, vol. 22, no. 8, Wiley-Blackwell, 2017, pp. 715–22, doi:10.1111/gtc.12508. short: X. Geng, T. Maruo, K. Mandai, I. Supriyanto, M. Miyata, S. Sakakibara, A. Mizoguchi, Y. Takai, M. Mori, Genes to Cells 22 (2017) 715–722. date_created: 2018-12-11T11:48:02Z date_published: 2017-08-01T00:00:00Z date_updated: 2021-01-12T08:11:37Z day: '01' department: - _id: PeJo doi: 10.1111/gtc.12508 intvolume: ' 22' issue: '8' language: - iso: eng month: '08' oa_version: None page: 715 - 722 publication: Genes to Cells publication_identifier: issn: - '13569597' publication_status: published publisher: Wiley-Blackwell publist_id: '6987' quality_controlled: '1' scopus_import: 1 status: public title: Roles of afadin in functional differentiations of hippocampal mossy fiber synapse type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 22 year: '2017' ... --- _id: '1118' abstract: - lang: eng text: Sharp wave-ripple (SWR) oscillations play a key role in memory consolidation during non-rapid eye movement sleep, immobility, and consummatory behavior. However, whether temporally modulated synaptic excitation or inhibition underlies the ripples is controversial. To address this question, we performed simultaneous recordings of excitatory and inhibitory postsynaptic currents (EPSCs and IPSCs) and local field potentials (LFPs) in the CA1 region of awake mice in vivo. During SWRs, inhibition dominated over excitation, with a peak conductance ratio of 4.1 ± 0.5. Furthermore, the amplitude of SWR-associated IPSCs was positively correlated with SWR magnitude, whereas that of EPSCs was not. Finally, phase analysis indicated that IPSCs were phase-locked to individual ripple cycles, whereas EPSCs were uniformly distributed in phase space. Optogenetic inhibition indicated that PV+ interneurons provided a major contribution to SWR-associated IPSCs. Thus, phasic inhibition, but not excitation, shapes SWR oscillations in the hippocampal CA1 region in vivo. acknowledged_ssus: - _id: M-Shop - _id: ScienComp - _id: PreCl article_processing_charge: No author: - first_name: Jian full_name: Gan, Jian id: 3614E438-F248-11E8-B48F-1D18A9856A87 last_name: Gan - first_name: Shih-Ming full_name: Weng, Shih-Ming id: 2F9C5AC8-F248-11E8-B48F-1D18A9856A87 last_name: Weng - first_name: Alejandro full_name: Pernia-Andrade, Alejandro id: 36963E98-F248-11E8-B48F-1D18A9856A87 last_name: Pernia-Andrade - first_name: Jozsef L full_name: Csicsvari, Jozsef L id: 3FA14672-F248-11E8-B48F-1D18A9856A87 last_name: Csicsvari orcid: 0000-0002-5193-4036 - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Gan J, Weng S-M, Pernia-Andrade A, Csicsvari JL, Jonas PM. Phase-locked inhibition, but not excitation, underlies hippocampal ripple oscillations in awake mice in vivo. Neuron. 2017;93(2):308-314. doi:10.1016/j.neuron.2016.12.018 apa: Gan, J., Weng, S.-M., Pernia-Andrade, A., Csicsvari, J. L., & Jonas, P. M. (2017). Phase-locked inhibition, but not excitation, underlies hippocampal ripple oscillations in awake mice in vivo. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2016.12.018 chicago: Gan, Jian, Shih-Ming Weng, Alejandro Pernia-Andrade, Jozsef L Csicsvari, and Peter M Jonas. “Phase-Locked Inhibition, but Not Excitation, Underlies Hippocampal Ripple Oscillations in Awake Mice in Vivo.” Neuron. Elsevier, 2017. https://doi.org/10.1016/j.neuron.2016.12.018. ieee: J. Gan, S.-M. Weng, A. Pernia-Andrade, J. L. Csicsvari, and P. M. Jonas, “Phase-locked inhibition, but not excitation, underlies hippocampal ripple oscillations in awake mice in vivo,” Neuron, vol. 93, no. 2. Elsevier, pp. 308–314, 2017. ista: Gan J, Weng S-M, Pernia-Andrade A, Csicsvari JL, Jonas PM. 2017. Phase-locked inhibition, but not excitation, underlies hippocampal ripple oscillations in awake mice in vivo. Neuron. 93(2), 308–314. mla: Gan, Jian, et al. “Phase-Locked Inhibition, but Not Excitation, Underlies Hippocampal Ripple Oscillations in Awake Mice in Vivo.” Neuron, vol. 93, no. 2, Elsevier, 2017, pp. 308–14, doi:10.1016/j.neuron.2016.12.018. short: J. Gan, S.-M. Weng, A. Pernia-Andrade, J.L. Csicsvari, P.M. Jonas, Neuron 93 (2017) 308–314. date_created: 2018-12-11T11:50:15Z date_published: 2017-01-18T00:00:00Z date_updated: 2023-09-20T11:31:48Z day: '18' ddc: - '571' department: - _id: PeJo - _id: JoCs doi: 10.1016/j.neuron.2016.12.018 ec_funded: 1 external_id: isi: - '000396428200010' file: - access_level: open_access content_type: application/pdf creator: system date_created: 2018-12-12T10:08:56Z date_updated: 2018-12-12T10:08:56Z file_id: '4719' file_name: IST-2017-752-v1+1_1-s2.0-S0896627316309606-main.pdf file_size: 2738950 relation: main_file file_date_updated: 2018-12-12T10:08:56Z has_accepted_license: '1' intvolume: ' 93' isi: 1 issue: '2' language: - iso: eng month: '01' oa: 1 oa_version: Published Version page: 308 - 314 project: - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons publication: Neuron publication_status: published publisher: Elsevier publist_id: '6244' pubrep_id: '752' quality_controlled: '1' scopus_import: '1' status: public title: Phase-locked inhibition, but not excitation, underlies hippocampal ripple oscillations in awake mice in vivo tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 93 year: '2017' ... --- _id: '1117' abstract: - lang: eng text: 'GABAergic synapses in brain circuits generate inhibitory output signals with submillisecond latency and temporal precision. Whether the molecular identity of the release sensor contributes to these signaling properties remains unclear. Here, we examined the Ca^2+ sensor of exocytosis at GABAergic basket cell (BC) to Purkinje cell (PC) synapses in cerebellum. Immunolabeling suggested that BC terminals selectively expressed synaptotagmin 2 (Syt2), whereas synaptotagmin 1 (Syt1) was enriched in excitatory terminals. Genetic elimination of Syt2 reduced action potential-evoked release to ∼10%, identifying Syt2 as the major Ca^2+ sensor at BC-PC synapses. Differential adenovirus-mediated rescue revealed that Syt2 triggered release with shorter latency and higher temporal precision and mediated faster vesicle pool replenishment than Syt1. Furthermore, deletion of Syt2 severely reduced and delayed disynaptic inhibition following parallel fiber stimulation. Thus, the selective use of Syt2 as release sensor at BC-PC synapses ensures fast and efficient feedforward inhibition in cerebellar microcircuits. #bioimagingfacility-author' acknowledged_ssus: - _id: Bio - _id: PreCl article_processing_charge: No author: - first_name: Chong full_name: Chen, Chong id: 3DFD581A-F248-11E8-B48F-1D18A9856A87 last_name: Chen - first_name: Itaru full_name: Arai, Itaru id: 32A73F6C-F248-11E8-B48F-1D18A9856A87 last_name: Arai - first_name: Rachel full_name: Satterield, Rachel last_name: Satterield - first_name: Samuel full_name: Young, Samuel last_name: Young - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Chen C, Arai itaru, Satterield R, Young S, Jonas PM. Synaptotagmin 2 is the fast Ca2+ sensor at a central inhibitory synapse. Cell Reports. 2017;18(3):723-736. doi:10.1016/j.celrep.2016.12.067 apa: Chen, C., Arai, itaru, Satterield, R., Young, S., & Jonas, P. M. (2017). Synaptotagmin 2 is the fast Ca2+ sensor at a central inhibitory synapse. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2016.12.067 chicago: Chen, Chong, itaru Arai, Rachel Satterield, Samuel Young, and Peter M Jonas. “Synaptotagmin 2 Is the Fast Ca2+ Sensor at a Central Inhibitory Synapse.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2016.12.067. ieee: C. Chen, itaru Arai, R. Satterield, S. Young, and P. M. Jonas, “Synaptotagmin 2 is the fast Ca2+ sensor at a central inhibitory synapse,” Cell Reports, vol. 18, no. 3. Cell Press, pp. 723–736, 2017. ista: Chen C, Arai itaru, Satterield R, Young S, Jonas PM. 2017. Synaptotagmin 2 is the fast Ca2+ sensor at a central inhibitory synapse. Cell Reports. 18(3), 723–736. mla: Chen, Chong, et al. “Synaptotagmin 2 Is the Fast Ca2+ Sensor at a Central Inhibitory Synapse.” Cell Reports, vol. 18, no. 3, Cell Press, 2017, pp. 723–36, doi:10.1016/j.celrep.2016.12.067. short: C. Chen, itaru Arai, R. Satterield, S. Young, P.M. Jonas, Cell Reports 18 (2017) 723–736. date_created: 2018-12-11T11:50:14Z date_published: 2017-01-17T00:00:00Z date_updated: 2023-09-20T11:32:15Z day: '17' ddc: - '571' department: - _id: PeJo doi: 10.1016/j.celrep.2016.12.067 ec_funded: 1 external_id: isi: - '000396470600013' file: - access_level: open_access content_type: application/pdf creator: system date_created: 2018-12-12T10:16:09Z date_updated: 2018-12-12T10:16:09Z file_id: '5195' file_name: IST-2017-751-v1+1_1-s2.0-S2211124716317740-main.pdf file_size: 4427591 relation: main_file file_date_updated: 2018-12-12T10:16:09Z has_accepted_license: '1' intvolume: ' 18' isi: 1 issue: '3' language: - iso: eng month: '01' oa: 1 oa_version: Published Version page: 723 - 736 project: - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons publication: Cell Reports publication_identifier: issn: - '22111247' publication_status: published publisher: Cell Press publist_id: '6245' pubrep_id: '751' quality_controlled: '1' related_material: record: - id: '324' relation: dissertation_contains status: public scopus_import: '1' status: public title: Synaptotagmin 2 is the fast Ca2+ sensor at a central inhibitory synapse tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 18 year: '2017' ... --- _id: '991' abstract: - lang: eng text: Synaptotagmin 7 (Syt7) was originally identified as a slow Ca2+ sensor for lysosome fusion, but its function at fast synapses is controversial. The paper by Luo and Südhof (2017) in this issue of Neuron shows that at the calyx of Held in the auditory brainstem Syt7 triggers asynchronous release during stimulus trains, resulting in reliable and temporally precise high-frequency transmission. Thus, a slow Ca2+ sensor contributes to the fast signaling properties of the calyx synapse. article_processing_charge: No author: - first_name: Chong full_name: Chen, Chong id: 3DFD581A-F248-11E8-B48F-1D18A9856A87 last_name: Chen - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: 'Chen C, Jonas PM. Synaptotagmins: That’s why so many. Neuron. 2017;94(4):694-696. doi:10.1016/j.neuron.2017.05.011' apa: 'Chen, C., & Jonas, P. M. (2017). Synaptotagmins: That’s why so many. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2017.05.011' chicago: 'Chen, Chong, and Peter M Jonas. “Synaptotagmins: That’s Why so Many.” Neuron. Elsevier, 2017. https://doi.org/10.1016/j.neuron.2017.05.011.' ieee: 'C. Chen and P. M. Jonas, “Synaptotagmins: That’s why so many,” Neuron, vol. 94, no. 4. Elsevier, pp. 694–696, 2017.' ista: 'Chen C, Jonas PM. 2017. Synaptotagmins: That’s why so many. Neuron. 94(4), 694–696.' mla: 'Chen, Chong, and Peter M. Jonas. “Synaptotagmins: That’s Why so Many.” Neuron, vol. 94, no. 4, Elsevier, 2017, pp. 694–96, doi:10.1016/j.neuron.2017.05.011.' short: C. Chen, P.M. Jonas, Neuron 94 (2017) 694–696. date_created: 2018-12-11T11:49:34Z date_published: 2017-05-17T00:00:00Z date_updated: 2023-09-22T09:54:37Z day: '17' department: - _id: PeJo doi: 10.1016/j.neuron.2017.05.011 external_id: isi: - '000401415100002' intvolume: ' 94' isi: 1 issue: '4' language: - iso: eng month: '05' oa_version: None page: 694 - 696 publication: Neuron publication_identifier: issn: - '08966273' publication_status: published publisher: Elsevier publist_id: '6408' quality_controlled: '1' scopus_import: '1' status: public title: 'Synaptotagmins: That’s why so many' type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 94 year: '2017' ... --- _id: '800' abstract: - lang: eng text: Gamma oscillations (30–150 Hz) in neuronal networks are associated with the processing and recall of information. We measured local field potentials in the dentate gyrus of freely moving mice and found that gamma activity occurs in bursts, which are highly heterogeneous in their spatial extensions, ranging from focal to global coherent events. Synaptic communication among perisomatic-inhibitory interneurons (PIIs) is thought to play an important role in the generation of hippocampal gamma patterns. However, how neuronal circuits can generate synchronous oscillations at different spatial scales is unknown. We analyzed paired recordings in dentate gyrus slices and show that synaptic signaling at interneuron-interneuron synapses is distance dependent. Synaptic strength declines whereas the duration of inhibitory signals increases with axonal distance among interconnected PIIs. Using neuronal network modeling, we show that distance-dependent inhibition generates multiple highly synchronous focal gamma bursts allowing the network to process complex inputs in parallel in flexibly organized neuronal centers. article_number: '758' article_processing_charge: No author: - first_name: Michael full_name: Strüber, Michael last_name: Strüber - first_name: Jonas full_name: Sauer, Jonas last_name: Sauer - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 - first_name: Marlene full_name: Bartos, Marlene last_name: Bartos citation: ama: Strüber M, Sauer J, Jonas PM, Bartos M. Distance-dependent inhibition facilitates focality of gamma oscillations in the dentate gyrus. Nature Communications. 2017;8(1). doi:10.1038/s41467-017-00936-3 apa: Strüber, M., Sauer, J., Jonas, P. M., & Bartos, M. (2017). Distance-dependent inhibition facilitates focality of gamma oscillations in the dentate gyrus. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/s41467-017-00936-3 chicago: Strüber, Michael, Jonas Sauer, Peter M Jonas, and Marlene Bartos. “Distance-Dependent Inhibition Facilitates Focality of Gamma Oscillations in the Dentate Gyrus.” Nature Communications. Nature Publishing Group, 2017. https://doi.org/10.1038/s41467-017-00936-3. ieee: M. Strüber, J. Sauer, P. M. Jonas, and M. Bartos, “Distance-dependent inhibition facilitates focality of gamma oscillations in the dentate gyrus,” Nature Communications, vol. 8, no. 1. Nature Publishing Group, 2017. ista: Strüber M, Sauer J, Jonas PM, Bartos M. 2017. Distance-dependent inhibition facilitates focality of gamma oscillations in the dentate gyrus. Nature Communications. 8(1), 758. mla: Strüber, Michael, et al. “Distance-Dependent Inhibition Facilitates Focality of Gamma Oscillations in the Dentate Gyrus.” Nature Communications, vol. 8, no. 1, 758, Nature Publishing Group, 2017, doi:10.1038/s41467-017-00936-3. short: M. Strüber, J. Sauer, P.M. Jonas, M. Bartos, Nature Communications 8 (2017). date_created: 2018-12-11T11:48:34Z date_published: 2017-10-02T00:00:00Z date_updated: 2023-09-27T10:59:41Z day: '02' ddc: - '571' department: - _id: PeJo doi: 10.1038/s41467-017-00936-3 ec_funded: 1 external_id: isi: - '000412053100004' file: - access_level: open_access checksum: 7e2c7621afd5f802338e92e8619f024d content_type: application/pdf creator: system date_created: 2018-12-12T10:15:17Z date_updated: 2020-07-14T12:48:07Z file_id: '5135' file_name: IST-2017-914-v1+1_s41467-017-00936-3.pdf file_size: 4261832 relation: main_file file_date_updated: 2020-07-14T12:48:07Z has_accepted_license: '1' intvolume: ' 8' isi: 1 issue: '1' language: - iso: eng month: '10' oa: 1 oa_version: Published Version project: - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons publication: Nature Communications publication_identifier: issn: - '20411723' publication_status: published publisher: Nature Publishing Group publist_id: '6853' pubrep_id: '914' quality_controlled: '1' scopus_import: '1' status: public title: Distance-dependent inhibition facilitates focality of gamma oscillations in the dentate gyrus tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 8 year: '2017' ... --- _id: '749' abstract: - lang: eng text: 'Synaptotagmin 7 (Syt7) is thought to be a Ca2+ sensor that mediates asynchronous transmitter release and facilitation at synapses. However, Syt7 is strongly expressed in fast-spiking, parvalbumin-expressing GABAergic interneurons, and the output synapses of these neurons produce only minimal asynchronous release and show depression rather than facilitation. To resolve this apparent contradiction, we examined the effects of genetic elimination of Syt7 on synaptic transmission at the GABAergic basket cell (BC)-Purkinje cell (PC) synapse in cerebellum. Our results indicate that at the BC-PC synapse, Syt7 contributes to asynchronous release, pool replenishment, and facilitation. In combination, these three effects ensure efficient transmitter release during high-frequency activity and guarantee frequency independence of inhibition. Our results identify a distinct function of Syt7: ensuring the efficiency of high-frequency inhibitory synaptic transmission' acknowledged_ssus: - _id: PreCl article_processing_charge: No author: - first_name: Chong full_name: Chen, Chong id: 3DFD581A-F248-11E8-B48F-1D18A9856A87 last_name: Chen - first_name: Rachel full_name: Satterfield, Rachel last_name: Satterfield - first_name: Samuel full_name: Young, Samuel last_name: Young - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Chen C, Satterfield R, Young S, Jonas PM. Triple function of Synaptotagmin 7 ensures efficiency of high-frequency transmission at central GABAergic synapses. Cell Reports. 2017;21(8):2082-2089. doi:10.1016/j.celrep.2017.10.122 apa: Chen, C., Satterfield, R., Young, S., & Jonas, P. M. (2017). Triple function of Synaptotagmin 7 ensures efficiency of high-frequency transmission at central GABAergic synapses. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.10.122 chicago: Chen, Chong, Rachel Satterfield, Samuel Young, and Peter M Jonas. “Triple Function of Synaptotagmin 7 Ensures Efficiency of High-Frequency Transmission at Central GABAergic Synapses.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.10.122. ieee: C. Chen, R. Satterfield, S. Young, and P. M. Jonas, “Triple function of Synaptotagmin 7 ensures efficiency of high-frequency transmission at central GABAergic synapses,” Cell Reports, vol. 21, no. 8. Cell Press, pp. 2082–2089, 2017. ista: Chen C, Satterfield R, Young S, Jonas PM. 2017. Triple function of Synaptotagmin 7 ensures efficiency of high-frequency transmission at central GABAergic synapses. Cell Reports. 21(8), 2082–2089. mla: Chen, Chong, et al. “Triple Function of Synaptotagmin 7 Ensures Efficiency of High-Frequency Transmission at Central GABAergic Synapses.” Cell Reports, vol. 21, no. 8, Cell Press, 2017, pp. 2082–89, doi:10.1016/j.celrep.2017.10.122. short: C. Chen, R. Satterfield, S. Young, P.M. Jonas, Cell Reports 21 (2017) 2082–2089. date_created: 2018-12-11T11:48:18Z date_published: 2017-11-21T00:00:00Z date_updated: 2023-09-27T12:26:04Z day: '21' ddc: - '570' - '571' department: - _id: PeJo doi: 10.1016/j.celrep.2017.10.122 ec_funded: 1 external_id: isi: - '000416216700007' file: - access_level: open_access checksum: a6afa3764909bf6edafa07982d8e1cee content_type: application/pdf creator: system date_created: 2018-12-12T10:09:14Z date_updated: 2020-07-14T12:47:59Z file_id: '4737' file_name: IST-2017-874-v1+1_PIIS2211124717316029.pdf file_size: 2759195 relation: main_file file_date_updated: 2020-07-14T12:47:59Z has_accepted_license: '1' intvolume: ' 21' isi: 1 issue: '8' language: - iso: eng month: '11' oa: 1 oa_version: Published Version page: 2082 - 2089 project: - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses - _id: 25B7EB9E-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '692692' name: Biophysics and circuit function of a giant cortical glumatergic synapse publication: Cell Reports publication_identifier: issn: - '22111247' publication_status: published publisher: Cell Press publist_id: '6907' pubrep_id: '874' quality_controlled: '1' related_material: record: - id: '324' relation: dissertation_contains status: public scopus_import: '1' status: public title: Triple function of Synaptotagmin 7 ensures efficiency of high-frequency transmission at central GABAergic synapses tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 21 year: '2017' ... --- _id: '1142' abstract: - lang: eng text: Hemolysis drives susceptibility to bacterial infections and predicts poor outcome from sepsis. These detrimental effects are commonly considered to be a consequence of heme-iron serving as a nutrient for bacteria. We employed a Gram-negative sepsis model and found that elevated heme levels impaired the control of bacterial proliferation independently of heme-iron acquisition by pathogens. Heme strongly inhibited phagocytosis and the migration of human and mouse phagocytes by disrupting actin cytoskeletal dynamics via activation of the GTP-binding Rho family protein Cdc42 by the guanine nucleotide exchange factor DOCK8. A chemical screening approach revealed that quinine effectively prevented heme effects on the cytoskeleton, restored phagocytosis and improved survival in sepsis. These mechanistic insights provide potential therapeutic targets for patients with sepsis or hemolytic disorders. acknowledgement: 'Y. Fukui (Medical Institute of Bioregulation, Kyushu University) and J. Stein (Theodor Kocher Institute, University of Bern) are acknowledged for providing the DOCK8 deficient bone marrow. and H. Häcker (St. Judes Children''s Research Hospital) for providing the ERHBD-HoxB8-encoding retroviral construct. pSpCas9(BB)-2a-Puro (PX459) was a gift from F. Zhang (Massachusetts Institute of Technology) (Addgene plasmid # 48139) and pGRG36 was a gift from N. Craig (Johns Hopkins University School of Medicine) (Addgene plasmid # 16666). LifeAct-GFP-encoding retrovirus was kindly provided by A. Leithner (Institute of Science and Technology Austria). pSIM8 and TKC E. coli were gifts from D.L. Court (Center for Cancer Research, National Cancer Institute). We acknowledge M. Gröger and S. Rauscher for excellent technical support (Core imaging facility, Medical University of Vienna). We thank D.P. Barlow and L.R. Cheever for critical reading of the manuscript. This work was supported by the Austrian Academy of Sciences, the Science Fund of the Austrian National Bank (14107) and the Austrian Science Fund FWF (I1620-B22) in the Infect-ERA framework (to S.Knapp).' author: - first_name: Rui full_name: Martins, Rui last_name: Martins - first_name: Julia full_name: Maier, Julia last_name: Maier - first_name: Anna full_name: Gorki, Anna last_name: Gorki - first_name: Kilian full_name: Huber, Kilian last_name: Huber - first_name: Omar full_name: Sharif, Omar last_name: Sharif - first_name: Philipp full_name: Starkl, Philipp last_name: Starkl - first_name: Simona full_name: Saluzzo, Simona last_name: Saluzzo - first_name: Federica full_name: Quattrone, Federica last_name: Quattrone - first_name: Riem full_name: Gawish, Riem last_name: Gawish - first_name: Karin full_name: Lakovits, Karin last_name: Lakovits - first_name: Michael full_name: Aichinger, Michael last_name: Aichinger - first_name: Branka full_name: Radic Sarikas, Branka last_name: Radic Sarikas - first_name: Charles full_name: Lardeau, Charles last_name: Lardeau - first_name: Anastasiya full_name: Hladik, Anastasiya last_name: Hladik - first_name: Ana full_name: Korosec, Ana last_name: Korosec - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 - first_name: Michelle full_name: Duggan, Michelle id: 2EDEA62C-F248-11E8-B48F-1D18A9856A87 last_name: Duggan - first_name: Dontscho full_name: Kerjaschki, Dontscho last_name: Kerjaschki - first_name: Harald full_name: Esterbauer, Harald last_name: Esterbauer - first_name: Jacques full_name: Colinge, Jacques last_name: Colinge - first_name: Stephanie full_name: Eisenbarth, Stephanie last_name: Eisenbarth - first_name: Thomas full_name: Decker, Thomas last_name: Decker - first_name: Keiryn full_name: Bennett, Keiryn last_name: Bennett - first_name: Stefan full_name: Kubicek, Stefan last_name: Kubicek - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Giulio full_name: Superti Furga, Giulio last_name: Superti Furga - first_name: Sylvia full_name: Knapp, Sylvia last_name: Knapp citation: ama: Martins R, Maier J, Gorki A, et al. Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. Nature Immunology. 2016;17(12):1361-1372. doi:10.1038/ni.3590 apa: Martins, R., Maier, J., Gorki, A., Huber, K., Sharif, O., Starkl, P., … Knapp, S. (2016). Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3590 chicago: Martins, Rui, Julia Maier, Anna Gorki, Kilian Huber, Omar Sharif, Philipp Starkl, Simona Saluzzo, et al. “Heme Drives Hemolysis-Induced Susceptibility to Infection via Disruption of Phagocyte Functions.” Nature Immunology. Nature Publishing Group, 2016. https://doi.org/10.1038/ni.3590. ieee: R. Martins et al., “Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions,” Nature Immunology, vol. 17, no. 12. Nature Publishing Group, pp. 1361–1372, 2016. ista: Martins R, Maier J, Gorki A, Huber K, Sharif O, Starkl P, Saluzzo S, Quattrone F, Gawish R, Lakovits K, Aichinger M, Radic Sarikas B, Lardeau C, Hladik A, Korosec A, Brown M, Vaahtomeri K, Duggan M, Kerjaschki D, Esterbauer H, Colinge J, Eisenbarth S, Decker T, Bennett K, Kubicek S, Sixt MK, Superti Furga G, Knapp S. 2016. Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. Nature Immunology. 17(12), 1361–1372. mla: Martins, Rui, et al. “Heme Drives Hemolysis-Induced Susceptibility to Infection via Disruption of Phagocyte Functions.” Nature Immunology, vol. 17, no. 12, Nature Publishing Group, 2016, pp. 1361–72, doi:10.1038/ni.3590. short: R. Martins, J. Maier, A. Gorki, K. Huber, O. Sharif, P. Starkl, S. Saluzzo, F. Quattrone, R. Gawish, K. Lakovits, M. Aichinger, B. Radic Sarikas, C. Lardeau, A. Hladik, A. Korosec, M. Brown, K. Vaahtomeri, M. Duggan, D. Kerjaschki, H. Esterbauer, J. Colinge, S. Eisenbarth, T. Decker, K. Bennett, S. Kubicek, M.K. Sixt, G. Superti Furga, S. Knapp, Nature Immunology 17 (2016) 1361–1372. date_created: 2018-12-11T11:50:22Z date_published: 2016-12-01T00:00:00Z date_updated: 2021-01-12T06:48:36Z day: '01' department: - _id: MiSi - _id: PeJo doi: 10.1038/ni.3590 intvolume: ' 17' issue: '12' language: - iso: eng main_file_link: - open_access: '1' url: https://ora.ox.ac.uk/objects/uuid:f53a464e-1e5b-4f08-a7d8-b6749b852b9d month: '12' oa: 1 oa_version: Submitted Version page: 1361 - 1372 publication: Nature Immunology publication_status: published publisher: Nature Publishing Group publist_id: '6216' quality_controlled: '1' scopus_import: 1 status: public title: Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 17 year: '2016' ... --- _id: '1323' abstract: - lang: eng text: Mossy fiber synapses on CA3 pyramidal cells are 'conditional detonators' that reliably discharge postsynaptic targets. The 'conditional' nature implies that burst activity in dentate gyrus granule cells is required for detonation. Whether single unitary excitatory postsynaptic potentials (EPSPs) trigger spikes in CA3 neurons remains unknown. Mossy fiber synapses exhibit both pronounced short-term facilitation and uniquely large post-tetanic potentiation (PTP). We tested whether PTP could convert mossy fiber synapses from subdetonator into detonator mode, using a recently developed method to selectively and noninvasively stimulate individual presynaptic terminals in rat brain slices. Unitary EPSPs failed to initiate a spike in CA3 neurons under control conditions, but reliably discharged them after induction of presynaptic short-term plasticity. Remarkably, PTP switched mossy fiber synapses into full detonators for tens of seconds. Plasticity-dependent detonation may be critical for efficient coding, storage, and recall of information in the granule cell–CA3 cell network. acknowledged_ssus: - _id: M-Shop - _id: PreCl article_number: e17977 author: - first_name: Nicholas full_name: Vyleta, Nicholas id: 36C4978E-F248-11E8-B48F-1D18A9856A87 last_name: Vyleta - first_name: Carolina full_name: Borges Merjane, Carolina id: 4305C450-F248-11E8-B48F-1D18A9856A87 last_name: Borges Merjane orcid: 0000-0003-0005-401X - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Vyleta N, Borges Merjane C, Jonas PM. Plasticity-dependent, full detonation at hippocampal mossy fiber–CA3 pyramidal neuron synapses. eLife. 2016;5. doi:10.7554/eLife.17977 apa: Vyleta, N., Borges Merjane, C., & Jonas, P. M. (2016). Plasticity-dependent, full detonation at hippocampal mossy fiber–CA3 pyramidal neuron synapses. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.17977 chicago: Vyleta, Nicholas, Carolina Borges Merjane, and Peter M Jonas. “Plasticity-Dependent, Full Detonation at Hippocampal Mossy Fiber–CA3 Pyramidal Neuron Synapses.” ELife. eLife Sciences Publications, 2016. https://doi.org/10.7554/eLife.17977. ieee: N. Vyleta, C. Borges Merjane, and P. M. Jonas, “Plasticity-dependent, full detonation at hippocampal mossy fiber–CA3 pyramidal neuron synapses,” eLife, vol. 5. eLife Sciences Publications, 2016. ista: Vyleta N, Borges Merjane C, Jonas PM. 2016. Plasticity-dependent, full detonation at hippocampal mossy fiber–CA3 pyramidal neuron synapses. eLife. 5, e17977. mla: Vyleta, Nicholas, et al. “Plasticity-Dependent, Full Detonation at Hippocampal Mossy Fiber–CA3 Pyramidal Neuron Synapses.” ELife, vol. 5, e17977, eLife Sciences Publications, 2016, doi:10.7554/eLife.17977. short: N. Vyleta, C. Borges Merjane, P.M. Jonas, ELife 5 (2016). date_created: 2018-12-11T11:51:22Z date_published: 2016-10-25T00:00:00Z date_updated: 2023-02-21T10:34:24Z day: '25' ddc: - '571' - '572' department: - _id: PeJo doi: 10.7554/eLife.17977 ec_funded: 1 file: - access_level: open_access checksum: a7201280c571bed88ebd459ce5ce6a47 content_type: application/pdf creator: system date_created: 2018-12-12T10:17:05Z date_updated: 2020-07-14T12:44:44Z file_id: '5257' file_name: IST-2016-715-v1+1_e17977-download.pdf file_size: 1477891 relation: main_file file_date_updated: 2020-07-14T12:44:44Z has_accepted_license: '1' intvolume: ' 5' language: - iso: eng month: '10' oa: 1 oa_version: Published Version project: - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons - _id: 25B7EB9E-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '692692' name: Biophysics and circuit function of a giant cortical glumatergic synapse publication: eLife publication_status: published publisher: eLife Sciences Publications publist_id: '5947' pubrep_id: '715' quality_controlled: '1' scopus_import: 1 status: public title: Plasticity-dependent, full detonation at hippocampal mossy fiber–CA3 pyramidal neuron synapses tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 5 year: '2016' ... --- _id: '1350' abstract: - lang: eng text: "The hippocampal CA3 region plays a key role in learning and memory. Recurrent CA3–CA3\r\nsynapses are thought to be the subcellular substrate of pattern completion. However, the\r\nsynaptic mechanisms of this network computation remain enigmatic. To investigate these mechanisms, we combined functional connectivity analysis with network modeling.\r\nSimultaneous recording fromup to eight CA3 pyramidal neurons revealed that connectivity was sparse, spatially uniform, and highly enriched in disynaptic motifs (reciprocal, convergence,divergence, and chain motifs). Unitary connections were composed of one or two synaptic contacts, suggesting efficient use of postsynaptic space. Real-size modeling indicated that CA3 networks with sparse connectivity, disynaptic motifs, and single-contact connections robustly generated pattern completion.Thus, macro- and microconnectivity contribute to efficient\r\nmemory storage and retrieval in hippocampal networks." acknowledged_ssus: - _id: ScienComp author: - first_name: José full_name: Guzmán, José id: 30CC5506-F248-11E8-B48F-1D18A9856A87 last_name: Guzmán - first_name: Alois full_name: Schlögl, Alois id: 45BF87EE-F248-11E8-B48F-1D18A9856A87 last_name: Schlögl orcid: 0000-0002-5621-8100 - first_name: Michael full_name: Frotscher, Michael last_name: Frotscher - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Guzmán J, Schlögl A, Frotscher M, Jonas PM. Synaptic mechanisms of pattern completion in the hippocampal CA3 network. Science. 2016;353(6304):1117-1123. doi:10.1126/science.aaf1836 apa: Guzmán, J., Schlögl, A., Frotscher, M., & Jonas, P. M. (2016). Synaptic mechanisms of pattern completion in the hippocampal CA3 network. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.aaf1836 chicago: Guzmán, José, Alois Schlögl, Michael Frotscher, and Peter M Jonas. “Synaptic Mechanisms of Pattern Completion in the Hippocampal CA3 Network.” Science. American Association for the Advancement of Science, 2016. https://doi.org/10.1126/science.aaf1836. ieee: J. Guzmán, A. Schlögl, M. Frotscher, and P. M. Jonas, “Synaptic mechanisms of pattern completion in the hippocampal CA3 network,” Science, vol. 353, no. 6304. American Association for the Advancement of Science, pp. 1117–1123, 2016. ista: Guzmán J, Schlögl A, Frotscher M, Jonas PM. 2016. Synaptic mechanisms of pattern completion in the hippocampal CA3 network. Science. 353(6304), 1117–1123. mla: Guzmán, José, et al. “Synaptic Mechanisms of Pattern Completion in the Hippocampal CA3 Network.” Science, vol. 353, no. 6304, American Association for the Advancement of Science, 2016, pp. 1117–23, doi:10.1126/science.aaf1836. short: J. Guzmán, A. Schlögl, M. Frotscher, P.M. Jonas, Science 353 (2016) 1117–1123. date_created: 2018-12-11T11:51:31Z date_published: 2016-09-09T00:00:00Z date_updated: 2021-01-12T06:50:04Z day: '09' ddc: - '570' department: - _id: ScienComp - _id: PeJo doi: 10.1126/science.aaf1836 ec_funded: 1 file: - access_level: open_access checksum: 89caefa4e181424cbf0aecc835fcc5ec content_type: application/pdf creator: system date_created: 2018-12-12T10:12:27Z date_updated: 2020-07-14T12:44:46Z file_id: '4945' file_name: IST-2017-823-v1+1_aaf1836_CombinedPDF_v2-1.pdf file_size: 19408143 relation: main_file file_date_updated: 2020-07-14T12:44:46Z has_accepted_license: '1' intvolume: ' 353' issue: '6304' language: - iso: eng month: '09' oa: 1 oa_version: Preprint page: 1117 - 1123 project: - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses publication: Science publication_status: published publisher: American Association for the Advancement of Science publist_id: '5899' pubrep_id: '823' quality_controlled: '1' scopus_import: 1 status: public title: Synaptic mechanisms of pattern completion in the hippocampal CA3 network type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 353 year: '2016' ... --- _id: '1435' abstract: - lang: eng text: ATP released from neurons and astrocytes during neuronal activity or under pathophysiological circumstances is able to influence information flow in neuronal circuits by activation of ionotropic P2X and metabotropic P2Y receptors and subsequent modulation of cellular excitability, synaptic strength, and plasticity. In the present paper we review cellular and network effects of P2Y receptors in the brain. We show that P2Y receptors inhibit the release of neurotransmitters, modulate voltage- and ligand-gated ion channels, and differentially influence the induction of synaptic plasticity in the prefrontal cortex, hippocampus, and cerebellum. The findings discussed here may explain how P2Y1 receptor activation during brain injury, hypoxia, inflammation, schizophrenia, or Alzheimer's disease leads to an impairment of cognitive processes. Hence, it is suggested that the blockade of P2Y1 receptors may have therapeutic potential against cognitive disturbances in these states. article_number: '1207393' author: - first_name: José full_name: Guzmán, José id: 30CC5506-F248-11E8-B48F-1D18A9856A87 last_name: Guzmán - first_name: Zoltan full_name: Gerevich, Zoltan last_name: Gerevich citation: ama: 'Guzmán J, Gerevich Z. P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction. Neural Plasticity. 2016;2016. doi:10.1155/2016/1207393' apa: 'Guzmán, J., & Gerevich, Z. (2016). P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction. Neural Plasticity. Hindawi Publishing Corporation. https://doi.org/10.1155/2016/1207393' chicago: 'Guzmán, José, and Zoltan Gerevich. “P2Y Receptors in Synaptic Transmission and Plasticity: Therapeutic Potential in Cognitive Dysfunction.” Neural Plasticity. Hindawi Publishing Corporation, 2016. https://doi.org/10.1155/2016/1207393.' ieee: 'J. Guzmán and Z. Gerevich, “P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction,” Neural Plasticity, vol. 2016. Hindawi Publishing Corporation, 2016.' ista: 'Guzmán J, Gerevich Z. 2016. P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction. Neural Plasticity. 2016, 1207393.' mla: 'Guzmán, José, and Zoltan Gerevich. “P2Y Receptors in Synaptic Transmission and Plasticity: Therapeutic Potential in Cognitive Dysfunction.” Neural Plasticity, vol. 2016, 1207393, Hindawi Publishing Corporation, 2016, doi:10.1155/2016/1207393.' short: J. Guzmán, Z. Gerevich, Neural Plasticity 2016 (2016). date_created: 2018-12-11T11:52:00Z date_published: 2016-01-01T00:00:00Z date_updated: 2021-01-12T06:50:43Z day: '01' ddc: - '570' department: - _id: PeJo doi: 10.1155/2016/1207393 file: - access_level: open_access checksum: 8dc5c2f3d44d4775a6e7e3edb0d7a0da content_type: application/pdf creator: system date_created: 2018-12-12T10:09:17Z date_updated: 2020-07-14T12:44:54Z file_id: '4740' file_name: IST-2016-580-v1+1_1207393.pdf file_size: 1395180 relation: main_file file_date_updated: 2020-07-14T12:44:54Z has_accepted_license: '1' intvolume: ' 2016' language: - iso: eng month: '01' oa: 1 oa_version: Published Version publication: Neural Plasticity publication_status: published publisher: Hindawi Publishing Corporation publist_id: '5762' pubrep_id: '580' quality_controlled: '1' scopus_import: 1 status: public title: 'P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction' tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 2016 year: '2016' ... --- _id: '12903' article_processing_charge: No author: - first_name: Alois full_name: Schlögl, Alois id: 45BF87EE-F248-11E8-B48F-1D18A9856A87 last_name: Schlögl orcid: 0000-0002-5621-8100 - first_name: Stephan full_name: Stadlbauer, Stephan id: 4D0BC184-F248-11E8-B48F-1D18A9856A87 last_name: Stadlbauer citation: ama: 'Schlögl A, Stadlbauer S. High performance computing at IST Austria: Modelling the human hippocampus. In: AHPC16 - Austrian HPC Meeting 2016. VSC - Vienna Scientific Cluster; 2016:37.' apa: 'Schlögl, A., & Stadlbauer, S. (2016). High performance computing at IST Austria: Modelling the human hippocampus. In AHPC16 - Austrian HPC Meeting 2016 (p. 37). Grundlsee, Austria: VSC - Vienna Scientific Cluster.' chicago: 'Schlögl, Alois, and Stephan Stadlbauer. “High Performance Computing at IST Austria: Modelling the Human Hippocampus.” In AHPC16 - Austrian HPC Meeting 2016, 37. VSC - Vienna Scientific Cluster, 2016.' ieee: 'A. Schlögl and S. Stadlbauer, “High performance computing at IST Austria: Modelling the human hippocampus,” in AHPC16 - Austrian HPC Meeting 2016, Grundlsee, Austria, 2016, p. 37.' ista: 'Schlögl A, Stadlbauer S. 2016. High performance computing at IST Austria: Modelling the human hippocampus. AHPC16 - Austrian HPC Meeting 2016. AHPC: Austrian HPC Meeting, 37.' mla: 'Schlögl, Alois, and Stephan Stadlbauer. “High Performance Computing at IST Austria: Modelling the Human Hippocampus.” AHPC16 - Austrian HPC Meeting 2016, VSC - Vienna Scientific Cluster, 2016, p. 37.' short: A. Schlögl, S. Stadlbauer, in:, AHPC16 - Austrian HPC Meeting 2016, VSC - Vienna Scientific Cluster, 2016, p. 37. conference: end_date: 2016-02-24 location: Grundlsee, Austria name: 'AHPC: Austrian HPC Meeting' start_date: 2016-02-22 date_created: 2023-05-05T12:54:47Z date_published: 2016-02-24T00:00:00Z date_updated: 2023-05-16T07:15:14Z day: '24' ddc: - '000' department: - _id: ScienComp - _id: PeJo file: - access_level: open_access checksum: 4a7b00362e81358d568f5e216fa03c3e content_type: application/pdf creator: dernst date_created: 2023-05-16T07:03:56Z date_updated: 2023-05-16T07:03:56Z file_id: '12968' file_name: 2016_AHPC_Schloegl.pdf file_size: 1073523 relation: main_file success: 1 file_date_updated: 2023-05-16T07:03:56Z has_accepted_license: '1' language: - iso: eng main_file_link: - open_access: '1' url: https://vsc.ac.at/fileadmin/user_upload/vsc/conferences/ahpc16/BOOKLET_AHPC16.pdf month: '02' oa: 1 oa_version: Published Version page: '37' publication: AHPC16 - Austrian HPC Meeting 2016 publication_status: published publisher: VSC - Vienna Scientific Cluster quality_controlled: '1' status: public title: 'High performance computing at IST Austria: Modelling the human hippocampus' type: conference_abstract user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2016' ... --- _id: '1432' abstract: - lang: eng text: CA3–CA3 recurrent excitatory synapses are thought to play a key role in memory storage and pattern completion. Whether the plasticity properties of these synapses are consistent with their proposed network functions remains unclear. Here, we examine the properties of spike timing-dependent plasticity (STDP) at CA3–CA3 synapses. Low-frequency pairing of excitatory postsynaptic potentials (EPSPs) and action potentials (APs) induces long-term potentiation (LTP), independent of temporal order. The STDP curve is symmetric and broad (half-width ~150 ms). Consistent with these STDP induction properties, AP–EPSP sequences lead to supralinear summation of spine [Ca2+] transients. Furthermore, afterdepolarizations (ADPs) following APs efficiently propagate into dendrites of CA3 pyramidal neurons, and EPSPs summate with dendritic ADPs. In autoassociative network models, storage and recall are more robust with symmetric than with asymmetric STDP rules. Thus, a specialized STDP induction rule allows reliable storage and recall of information in the hippocampal CA3 network. acknowledgement: 'We thank Jozsef Csicsvari and Nelson Spruston for critically reading the manuscript. We also thank A. Schlögl for programming, F. Marr for technical assistance and E. Kramberger for manuscript editing. ' article_number: '11552' author: - first_name: Rajiv Kumar full_name: Mishra, Rajiv Kumar id: 46CB58F2-F248-11E8-B48F-1D18A9856A87 last_name: Mishra - first_name: Sooyun full_name: Kim, Sooyun id: 394AB1C8-F248-11E8-B48F-1D18A9856A87 last_name: Kim - first_name: José full_name: Guzmán, José id: 30CC5506-F248-11E8-B48F-1D18A9856A87 last_name: Guzmán orcid: 0000-0003-2209-5242 - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Mishra RK, Kim S, Guzmán J, Jonas PM. Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative networks. Nature Communications. 2016;7. doi:10.1038/ncomms11552 apa: Mishra, R. K., Kim, S., Guzmán, J., & Jonas, P. M. (2016). Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative networks. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms11552 chicago: Mishra, Rajiv Kumar, Sooyun Kim, José Guzmán, and Peter M Jonas. “Symmetric Spike Timing-Dependent Plasticity at CA3–CA3 Synapses Optimizes Storage and Recall in Autoassociative Networks.” Nature Communications. Nature Publishing Group, 2016. https://doi.org/10.1038/ncomms11552. ieee: R. K. Mishra, S. Kim, J. Guzmán, and P. M. Jonas, “Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative networks,” Nature Communications, vol. 7. Nature Publishing Group, 2016. ista: Mishra RK, Kim S, Guzmán J, Jonas PM. 2016. Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative networks. Nature Communications. 7, 11552. mla: Mishra, Rajiv Kumar, et al. “Symmetric Spike Timing-Dependent Plasticity at CA3–CA3 Synapses Optimizes Storage and Recall in Autoassociative Networks.” Nature Communications, vol. 7, 11552, Nature Publishing Group, 2016, doi:10.1038/ncomms11552. short: R.K. Mishra, S. Kim, J. Guzmán, P.M. Jonas, Nature Communications 7 (2016). date_created: 2018-12-11T11:51:59Z date_published: 2016-05-13T00:00:00Z date_updated: 2023-09-07T11:55:25Z day: '13' ddc: - '570' department: - _id: PeJo doi: 10.1038/ncomms11552 ec_funded: 1 file: - access_level: open_access checksum: 7e84d0392348c874d473b62f1042de22 content_type: application/pdf creator: system date_created: 2018-12-12T10:18:33Z date_updated: 2020-07-14T12:44:53Z file_id: '5355' file_name: IST-2016-582-v1+1_ncomms11552.pdf file_size: 4510512 relation: main_file file_date_updated: 2020-07-14T12:44:53Z has_accepted_license: '1' intvolume: ' 7' language: - iso: eng month: '05' oa: 1 oa_version: Published Version project: - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons publication: Nature Communications publication_status: published publisher: Nature Publishing Group publist_id: '5766' pubrep_id: '582' quality_controlled: '1' related_material: record: - id: '1396' relation: dissertation_contains status: public scopus_import: 1 status: public title: Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative networks tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 7 year: '2016' ... --- _id: '1396' abstract: - lang: eng text: CA3 pyramidal neurons are thought to pay a key role in memory storage and pattern completion by activity-dependent synaptic plasticity between CA3-CA3 recurrent excitatory synapses. To examine the induction rules of synaptic plasticity at CA3-CA3 synapses, we performed whole-cell patch-clamp recordings in acute hippocampal slices from rats (postnatal 21-24 days) at room temperature. Compound excitatory postsynaptic potentials (ESPSs) were recorded by tract stimulation in stratum oriens in the presence of 10 µM gabazine. High-frequency stimulation (HFS) induced N-methyl-D-aspartate (NMDA) receptor-dependent long-term potentiation (LTP). Although LTP by HFS did not requier postsynaptic spikes, it was blocked by Na+-channel blockers suggesting that local active processes (e.g.) dendritic spikes) may contribute to LTP induction without requirement of a somatic action potential (AP). We next examined the properties of spike timing-dependent plasticity (STDP) at CA3-CA3 synapses. Unexpectedly, low-frequency pairing of EPSPs and backpropagated action potentialy (bAPs) induced LTP, independent of temporal order. The STDP curve was symmetric and broad, with a half-width of ~150 ms. Consistent with these specific STDP induction properties, post-presynaptic sequences led to a supralinear summation of spine [Ca2+] transients. Furthermore, in autoassociative network models, storage and recall was substantially more robust with symmetric than with asymmetric STDP rules. In conclusion, we found associative forms of LTP at CA3-CA3 recurrent collateral synapses with distinct induction rules. LTP induced by HFS may be associated with dendritic spikes. In contrast, low frequency pairing of pre- and postsynaptic activity induced LTP only if EPSP-AP were temporally very close. Together, these induction mechanisms of synaptiic plasticity may contribute to memory storage in the CA3-CA3 microcircuit at different ranges of activity. alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Rajiv Kumar full_name: Mishra, Rajiv Kumar id: 46CB58F2-F248-11E8-B48F-1D18A9856A87 last_name: Mishra citation: ama: Mishra RK. Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus. 2016. apa: Mishra, R. K. (2016). Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus. Institute of Science and Technology Austria. chicago: Mishra, Rajiv Kumar. “Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses in Hippocampus.” Institute of Science and Technology Austria, 2016. ieee: R. K. Mishra, “Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus,” Institute of Science and Technology Austria, 2016. ista: Mishra RK. 2016. Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus. Institute of Science and Technology Austria. mla: Mishra, Rajiv Kumar. Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses in Hippocampus. Institute of Science and Technology Austria, 2016. short: R.K. Mishra, Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses in Hippocampus, Institute of Science and Technology Austria, 2016. date_created: 2018-12-11T11:51:46Z date_published: 2016-03-01T00:00:00Z date_updated: 2023-09-07T11:55:26Z day: '01' ddc: - '570' degree_awarded: PhD department: - _id: PeJo file: - access_level: closed checksum: 5a010a838faf040f7064f3cfb802f743 content_type: application/pdf creator: dernst date_created: 2019-08-09T12:14:46Z date_updated: 2020-07-14T12:44:48Z file_id: '6782' file_name: Thesis_Mishra_Rajiv (Final).pdf file_size: 2407572 relation: main_file - access_level: open_access checksum: 81b26d9ede92c99f1d8cc6fa1d04cbbb content_type: application/pdf creator: dernst date_created: 2021-02-22T11:48:44Z date_updated: 2021-02-22T11:48:44Z file_id: '9183' file_name: 2016_RajivMishra_Thesis.pdf file_size: 2407572 relation: main_file success: 1 file_date_updated: 2021-02-22T11:48:44Z has_accepted_license: '1' language: - iso: eng month: '03' oa: 1 oa_version: Published Version page: '83' publication_identifier: issn: - 2663-337X publication_status: published publisher: Institute of Science and Technology Austria publist_id: '5811' related_material: record: - id: '1432' relation: part_of_dissertation status: public status: public supervisor: - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 title: Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus type: dissertation user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 year: '2016' ... --- _id: '1616' abstract: - lang: eng text: The hippocampus plays a key role in learning and memory. Previous studies suggested that the main types of principal neurons, dentate gyrus granule cells (GCs), CA3 pyramidal neurons, and CA1 pyramidal neurons, differ in their activity pattern, with sparse firing in GCs and more frequent firing in CA3 and CA1 pyramidal neurons. It has been assumed but never shown that such different activity may be caused by differential synaptic excitation. To test this hypothesis, we performed high-resolution whole-cell patch-clamp recordings in anesthetized rats in vivo. In contrast to previous in vitro data, both CA3 and CA1 pyramidal neurons fired action potentials spontaneously, with a frequency of ∼3–6 Hz, whereas GCs were silent. Furthermore, both CA3 and CA1 cells primarily fired in bursts. To determine the underlying mechanisms, we quantitatively assessed the frequency of spontaneous excitatory synaptic input, the passive membrane properties, and the active membrane characteristics. Surprisingly, GCs showed comparable synaptic excitation to CA3 and CA1 cells and the highest ratio of excitation versus hyperpolarizing inhibition. Thus, differential synaptic excitation is not responsible for differences in firing. Moreover, the three types of hippocampal neurons markedly differed in their passive properties. While GCs showed the most negative membrane potential, CA3 pyramidal neurons had the highest input resistance and the slowest membrane time constant. The three types of neurons also differed in the active membrane characteristics. GCs showed the highest action potential threshold, but displayed the largest gain of the input-output curves. In conclusion, our results reveal that differential firing of the three main types of hippocampal principal neurons in vivo is not primarily caused by differences in the characteristics of the synaptic input, but by the distinct properties of synaptic integration and input-output transformation. acknowledgement: "The authors thank Jose Guzman for critically reading prior versions of the manuscript. They also thank T. Asenov for\r\nengineering mechanical devices, A. Schlögl for efficient pro-gramming, F. Marr for technical assistance, and E. Kramberger for manuscript editing." article_processing_charge: No author: - first_name: Janina full_name: Kowalski, Janina id: 3F3CA136-F248-11E8-B48F-1D18A9856A87 last_name: Kowalski - first_name: Jian full_name: Gan, Jian id: 3614E438-F248-11E8-B48F-1D18A9856A87 last_name: Gan - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 - first_name: Alejandro full_name: Pernia-Andrade, Alejandro id: 36963E98-F248-11E8-B48F-1D18A9856A87 last_name: Pernia-Andrade citation: ama: Kowalski J, Gan J, Jonas PM, Pernia-Andrade A. Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats. Hippocampus. 2016;26(5):668-682. doi:10.1002/hipo.22550 apa: Kowalski, J., Gan, J., Jonas, P. M., & Pernia-Andrade, A. (2016). Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats. Hippocampus. Wiley. https://doi.org/10.1002/hipo.22550 chicago: Kowalski, Janina, Jian Gan, Peter M Jonas, and Alejandro Pernia-Andrade. “Intrinsic Membrane Properties Determine Hippocampal Differential Firing Pattern in Vivo in Anesthetized Rats.” Hippocampus. Wiley, 2016. https://doi.org/10.1002/hipo.22550. ieee: J. Kowalski, J. Gan, P. M. Jonas, and A. Pernia-Andrade, “Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats,” Hippocampus, vol. 26, no. 5. Wiley, pp. 668–682, 2016. ista: Kowalski J, Gan J, Jonas PM, Pernia-Andrade A. 2016. Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats. Hippocampus. 26(5), 668–682. mla: Kowalski, Janina, et al. “Intrinsic Membrane Properties Determine Hippocampal Differential Firing Pattern in Vivo in Anesthetized Rats.” Hippocampus, vol. 26, no. 5, Wiley, 2016, pp. 668–82, doi:10.1002/hipo.22550. short: J. Kowalski, J. Gan, P.M. Jonas, A. Pernia-Andrade, Hippocampus 26 (2016) 668–682. date_created: 2018-12-11T11:53:03Z date_published: 2016-05-01T00:00:00Z date_updated: 2023-10-17T10:02:02Z day: '01' ddc: - '570' department: - _id: PeJo doi: 10.1002/hipo.22550 file: - access_level: open_access checksum: 284b72b12fbe15474833ed3d4549f86b content_type: application/pdf creator: system date_created: 2018-12-12T10:13:47Z date_updated: 2020-07-14T12:45:07Z file_id: '5033' file_name: IST-2016-469-v1+1_Kowalski_et_al-Hippocampus.pdf file_size: 905348 relation: main_file file_date_updated: 2020-07-14T12:45:07Z has_accepted_license: '1' intvolume: ' 26' issue: '5' language: - iso: eng license: https://creativecommons.org/licenses/by-nc-nd/4.0/ month: '05' oa: 1 oa_version: Published Version page: 668 - 682 publication: Hippocampus publication_identifier: eissn: - 1098-1063 issn: - 1050-9631 publication_status: published publisher: Wiley publist_id: '5550' pubrep_id: '469' quality_controlled: '1' scopus_import: '1' status: public title: Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 26 year: '2016' ... --- _id: '1535' abstract: - lang: eng text: Neuronal and neuroendocrine L-type calcium channels (Cav1.2, Cav1.3) open readily at relatively low membrane potentials and allow Ca2+ to enter the cells near resting potentials. In this way, Cav1.2 and Cav1.3 shape the action potential waveform, contribute to gene expression, synaptic plasticity, neuronal differentiation, hormone secretion and pacemaker activity. In the chromaffin cells (CCs) of the adrenal medulla, Cav1.3 is highly expressed and is shown to support most of the pacemaking current that sustains action potential (AP) firings and part of the catecholamine secretion. Cav1.3 forms Ca2+-nanodomains with the fast inactivating BK channels and drives the resting SK currents. These latter set the inter-spike interval duration between consecutive spikes during spontaneous firing and the rate of spike adaptation during sustained depolarizations. Cav1.3 plays also a primary role in the switch from “tonic” to “burst” firing that occurs in mouse CCs when either the availability of voltage-gated Na channels (Nav) is reduced or the β2 subunit featuring the fast inactivating BK channels is deleted. Here, we discuss the functional role of these “neuronlike” firing modes in CCs and how Cav1.3 contributes to them. The open issue is to understand how these novel firing patterns are adapted to regulate the quantity of circulating catecholamines during resting condition or in response to acute and chronic stress. acknowledgement: This work was supported by the Italian MIUR (PRIN 2010/2011 project 2010JFYFY2) and the University of Torino. article_processing_charge: No article_type: original author: - first_name: David H full_name: Vandael, David H id: 3AE48E0A-F248-11E8-B48F-1D18A9856A87 last_name: Vandael orcid: 0000-0001-7577-1676 - first_name: Andrea full_name: Marcantoni, Andrea last_name: Marcantoni - first_name: Emilio full_name: Carbone, Emilio last_name: Carbone citation: ama: Vandael DH, Marcantoni A, Carbone E. Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells. Current Molecular Pharmacology. 2015;8(2):149-161. doi:10.2174/1874467208666150507105443 apa: Vandael, D. H., Marcantoni, A., & Carbone, E. (2015). Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells. Current Molecular Pharmacology. Bentham Science Publishers. https://doi.org/10.2174/1874467208666150507105443 chicago: Vandael, David H, Andrea Marcantoni, and Emilio Carbone. “Cav1.3 Channels as Key Regulators of Neuron-like Firings and Catecholamine Release in Chromaffin Cells.” Current Molecular Pharmacology. Bentham Science Publishers, 2015. https://doi.org/10.2174/1874467208666150507105443. ieee: D. H. Vandael, A. Marcantoni, and E. Carbone, “Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells,” Current Molecular Pharmacology, vol. 8, no. 2. Bentham Science Publishers, pp. 149–161, 2015. ista: Vandael DH, Marcantoni A, Carbone E. 2015. Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells. Current Molecular Pharmacology. 8(2), 149–161. mla: Vandael, David H., et al. “Cav1.3 Channels as Key Regulators of Neuron-like Firings and Catecholamine Release in Chromaffin Cells.” Current Molecular Pharmacology, vol. 8, no. 2, Bentham Science Publishers, 2015, pp. 149–61, doi:10.2174/1874467208666150507105443. short: D.H. Vandael, A. Marcantoni, E. Carbone, Current Molecular Pharmacology 8 (2015) 149–161. date_created: 2018-12-11T11:52:35Z date_published: 2015-10-01T00:00:00Z date_updated: 2021-01-12T06:51:26Z day: '01' department: - _id: PeJo doi: 10.2174/1874467208666150507105443 external_id: pmid: - '25966692' intvolume: ' 8' issue: '2' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384372/ month: '10' oa: 1 oa_version: Submitted Version page: 149 - 161 pmid: 1 publication: Current Molecular Pharmacology publication_status: published publisher: Bentham Science Publishers publist_id: '5636' quality_controlled: '1' scopus_import: 1 status: public title: Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 8 year: '2015' ... --- _id: '1565' abstract: - lang: eng text: Leptin is an adipokine produced by the adipose tissue regulating body weight through its appetite-suppressing effect. Besides being expressed in the hypothalamus and hippocampus, leptin receptors (ObRs) are also present in chromaffin cells of the adrenal medulla. In the present study, we report the effect of leptin on mouse chromaffin cell (MCC) functionality, focusing on cell excitability and catecholamine secretion. Acute application of leptin (1 nm) on spontaneously firing MCCs caused a slowly developing membrane hyperpolarization followed by complete blockade of action potential (AP) firing. This inhibitory effect at rest was abolished by the BK channel blocker paxilline (1 μm), suggesting the involvement of BK potassium channels. Single-channel recordings in 'perforated microvesicles' confirmed that leptin increased BK channel open probability without altering its unitary conductance. BK channel up-regulation was associated with the phosphoinositide 3-kinase (PI3K) signalling cascade because the PI3K specific inhibitor wortmannin (100 nm) fully prevented BK current increase. We also tested the effect of leptin on evoked AP firing and Ca2+-driven exocytosis. Although leptin preserves well-adapted AP trains of lower frequency, APs are broader and depolarization-evoked exocytosis is increased as a result of the larger size of the ready-releasable pool and higher frequency of vesicle release. The kinetics and quantal size of single secretory events remained unaltered. Leptin had no effect on firing and secretion in db-/db- mice lacking the ObR gene, confirming its specificity. In conclusion, leptin exhibits a dual action on MCC activity. It dampens AP firing at rest but preserves AP firing and increases catecholamine secretion during sustained stimulation, highlighting the importance of the adipo-adrenal axis in the leptin-mediated increase of sympathetic tone and catecholamine release. acknowledgement: "This work was supported by the Compagnia di San Paolo Foundation ‘Neuroscience Program’ to VC and ‘Progetto di Ateneo 2011-13’ to EC.\r\nWe thank Dr Claudio Franchino for cell preparation and for providing excellent technical support." author: - first_name: Daniela full_name: Gavello, Daniela last_name: Gavello - first_name: David H full_name: Vandael, David H id: 3AE48E0A-F248-11E8-B48F-1D18A9856A87 last_name: Vandael orcid: 0000-0001-7577-1676 - first_name: Sara full_name: Gosso, Sara last_name: Gosso - first_name: Emilio full_name: Carbone, Emilio last_name: Carbone - first_name: Valentina full_name: Carabelli, Valentina last_name: Carabelli citation: ama: Gavello D, Vandael DH, Gosso S, Carbone E, Carabelli V. Dual action of leptin on rest-firing and stimulated catecholamine release via phosphoinositide 3-kinase-riven BK channel up-regulation in mouse chromaffin cells. Journal of Physiology. 2015;593(22):4835-4853. doi:10.1113/JP271078 apa: Gavello, D., Vandael, D. H., Gosso, S., Carbone, E., & Carabelli, V. (2015). Dual action of leptin on rest-firing and stimulated catecholamine release via phosphoinositide 3-kinase-riven BK channel up-regulation in mouse chromaffin cells. Journal of Physiology. Wiley-Blackwell. https://doi.org/10.1113/JP271078 chicago: Gavello, Daniela, David H Vandael, Sara Gosso, Emilio Carbone, and Valentina Carabelli. “Dual Action of Leptin on Rest-Firing and Stimulated Catecholamine Release via Phosphoinositide 3-Kinase-Riven BK Channel up-Regulation in Mouse Chromaffin Cells.” Journal of Physiology. Wiley-Blackwell, 2015. https://doi.org/10.1113/JP271078. ieee: D. Gavello, D. H. Vandael, S. Gosso, E. Carbone, and V. Carabelli, “Dual action of leptin on rest-firing and stimulated catecholamine release via phosphoinositide 3-kinase-riven BK channel up-regulation in mouse chromaffin cells,” Journal of Physiology, vol. 593, no. 22. Wiley-Blackwell, pp. 4835–4853, 2015. ista: Gavello D, Vandael DH, Gosso S, Carbone E, Carabelli V. 2015. Dual action of leptin on rest-firing and stimulated catecholamine release via phosphoinositide 3-kinase-riven BK channel up-regulation in mouse chromaffin cells. Journal of Physiology. 593(22), 4835–4853. mla: Gavello, Daniela, et al. “Dual Action of Leptin on Rest-Firing and Stimulated Catecholamine Release via Phosphoinositide 3-Kinase-Riven BK Channel up-Regulation in Mouse Chromaffin Cells.” Journal of Physiology, vol. 593, no. 22, Wiley-Blackwell, 2015, pp. 4835–53, doi:10.1113/JP271078. short: D. Gavello, D.H. Vandael, S. Gosso, E. Carbone, V. Carabelli, Journal of Physiology 593 (2015) 4835–4853. date_created: 2018-12-11T11:52:45Z date_published: 2015-11-15T00:00:00Z date_updated: 2021-01-12T06:51:38Z day: '15' department: - _id: PeJo doi: 10.1113/JP271078 external_id: pmid: - '26282459' intvolume: ' 593' issue: '22' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4650409/ month: '11' oa: 1 oa_version: Submitted Version page: 4835 - 4853 pmid: 1 publication: Journal of Physiology publication_status: published publisher: Wiley-Blackwell publist_id: '5606' quality_controlled: '1' scopus_import: 1 status: public title: Dual action of leptin on rest-firing and stimulated catecholamine release via phosphoinositide 3-kinase-riven BK channel up-regulation in mouse chromaffin cells type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 593 year: '2015' ... --- _id: '1580' abstract: - lang: eng text: Synapsins (Syns) are an evolutionarily conserved family of presynaptic proteins crucial for the fine-tuning of synaptic function. A large amount of experimental evidences has shown that Syns are involved in the development of epileptic phenotypes and several mutations in Syn genes have been associated with epilepsy in humans and animal models. Syn mutations induce alterations in circuitry and neurotransmitter release, differentially affecting excitatory and inhibitory synapses, thus causing an excitation/inhibition imbalance in network excitability toward hyperexcitability that may be a determinant with regard to the development of epilepsy. Another approach to investigate epileptogenic mechanisms is to understand how silencing Syn affects the cellular behavior of single neurons and is associated with the hyperexcitable phenotypes observed in epilepsy. Here, we examined the functional effects of antisense-RNA inhibition of Syn expression on individually identified and isolated serotonergic cells of the Helix land snail. We found that Helix synapsin silencing increases cell excitability characterized by a slightly depolarized resting membrane potential, decreases the rheobase, reduces the threshold for action potential (AP) firing and increases the mean and instantaneous firing rates, with respect to control cells. The observed increase of Ca2+ and BK currents in Syn-silenced cells seems to be related to changes in the shape of the AP waveform. These currents sustain the faster spiking in Syn-deficient cells by increasing the after hyperpolarization and limiting the Na+ and Ca2+ channel inactivation during repetitive firing. This in turn speeds up the depolarization phase by reaching the AP threshold faster. Our results provide evidence that Syn silencing increases intrinsic cell excitability associated with increased Ca2+ and Ca2+-dependent BK currents in the absence of excitatory or inhibitory inputs. article_processing_charge: No article_type: original author: - first_name: Oscar full_name: Brenes, Oscar last_name: Brenes - first_name: David H full_name: Vandael, David H id: 3AE48E0A-F248-11E8-B48F-1D18A9856A87 last_name: Vandael orcid: 0000-0001-7577-1676 - first_name: Emilio full_name: Carbone, Emilio last_name: Carbone - first_name: Pier full_name: Montarolo, Pier last_name: Montarolo - first_name: Mirella full_name: Ghirardi, Mirella last_name: Ghirardi citation: ama: Brenes O, Vandael DH, Carbone E, Montarolo P, Ghirardi M. Knock-down of synapsin alters cell excitability and action potential waveform by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons. Neuroscience. 2015;311:430-443. doi:10.1016/j.neuroscience.2015.10.046 apa: Brenes, O., Vandael, D. H., Carbone, E., Montarolo, P., & Ghirardi, M. (2015). Knock-down of synapsin alters cell excitability and action potential waveform by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons. Neuroscience. Elsevier. https://doi.org/10.1016/j.neuroscience.2015.10.046 chicago: Brenes, Oscar, David H Vandael, Emilio Carbone, Pier Montarolo, and Mirella Ghirardi. “Knock-down of Synapsin Alters Cell Excitability and Action Potential Waveform by Potentiating BK and Voltage Gated Ca2 Currents in Helix Serotonergic Neurons.” Neuroscience. Elsevier, 2015. https://doi.org/10.1016/j.neuroscience.2015.10.046. ieee: O. Brenes, D. H. Vandael, E. Carbone, P. Montarolo, and M. Ghirardi, “Knock-down of synapsin alters cell excitability and action potential waveform by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons,” Neuroscience, vol. 311. Elsevier, pp. 430–443, 2015. ista: Brenes O, Vandael DH, Carbone E, Montarolo P, Ghirardi M. 2015. Knock-down of synapsin alters cell excitability and action potential waveform by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons. Neuroscience. 311, 430–443. mla: Brenes, Oscar, et al. “Knock-down of Synapsin Alters Cell Excitability and Action Potential Waveform by Potentiating BK and Voltage Gated Ca2 Currents in Helix Serotonergic Neurons.” Neuroscience, vol. 311, Elsevier, 2015, pp. 430–43, doi:10.1016/j.neuroscience.2015.10.046. short: O. Brenes, D.H. Vandael, E. Carbone, P. Montarolo, M. Ghirardi, Neuroscience 311 (2015) 430–443. date_created: 2018-12-11T11:52:50Z date_published: 2015-12-17T00:00:00Z date_updated: 2021-01-12T06:51:44Z day: '17' ddc: - '570' department: - _id: PeJo doi: 10.1016/j.neuroscience.2015.10.046 file: - access_level: open_access checksum: af2c4c994718c7be417eba0dc746aac9 content_type: application/pdf creator: dernst date_created: 2020-05-15T06:50:20Z date_updated: 2020-07-14T12:45:02Z file_id: '7849' file_name: 2015_Neuroscience_Brenes.pdf file_size: 5563015 relation: main_file file_date_updated: 2020-07-14T12:45:02Z has_accepted_license: '1' intvolume: ' 311' language: - iso: eng month: '12' oa: 1 oa_version: Submitted Version page: 430 - 443 publication: Neuroscience publication_status: published publisher: Elsevier publist_id: '5591' quality_controlled: '1' scopus_import: 1 status: public title: Knock-down of synapsin alters cell excitability and action potential waveform by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 311 year: '2015' ... --- _id: '1615' abstract: - lang: eng text: Loss-of-function mutations in the synaptic adhesion protein Neuroligin-4 are among the most common genetic abnormalities associated with autism spectrum disorders, but little is known about the function of Neuroligin-4 and the consequences of its loss. We assessed synaptic and network characteristics in Neuroligin-4 knockout mice, focusing on the hippocampus as a model brain region with a critical role in cognition and memory, and found that Neuroligin-4 deletion causes subtle defects of the protein composition and function of GABAergic synapses in the hippocampal CA3 region. Interestingly, these subtle synaptic changes are accompanied by pronounced perturbations of γ-oscillatory network activity, which has been implicated in cognitive function and is altered in multiple psychiatric and neurodevelopmental disorders. Our data provide important insights into the mechanisms by which Neuroligin-4-dependent GABAergic synapses may contribute to autism phenotypes and indicate new strategies for therapeutic approaches. acknowledgement: This work was supported by the Max Planck Society (N.B. and H.E.), the European Commission (EU-AIMS FP7-115300, N.B. and H.E.; Marie Curie IRG, D.K.-B.), the German Research Foundation (CNMPB, N.B., H.E., and F.V.), the Alexander von Humboldt-Foundation (D.K.-B.), and the Austrian Fond zur Förderung der Wissenschaftlichen Forschung (P 24909-B24, P.J.). M.H. was a student of the doctoral program Molecular Physiology of the Brain. Dr. J.-M. Fritschy generously provided the GABAARγ2 antibody. We thank F. Benseler, I. Thanhäuser, D. Schwerdtfeger, A. Ronnenberg, and D. Winkler for valuable advice and excellent technical support. We are grateful to the staff at the animal facility of the Max Planck Institute of Experimental Medicine for mouse husbandry. author: - first_name: Matthieu full_name: Hammer, Matthieu last_name: Hammer - first_name: Dilja full_name: Krueger Burg, Dilja last_name: Krueger Burg - first_name: Liam full_name: Tuffy, Liam last_name: Tuffy - first_name: Benjamin full_name: Cooper, Benjamin last_name: Cooper - first_name: Holger full_name: Taschenberger, Holger last_name: Taschenberger - first_name: Sarit full_name: Goswami, Sarit id: 3A578F32-F248-11E8-B48F-1D18A9856A87 last_name: Goswami - first_name: Hannelore full_name: Ehrenreich, Hannelore last_name: Ehrenreich - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 - first_name: Frederique full_name: Varoqueaux, Frederique last_name: Varoqueaux - first_name: Jeong full_name: Rhee, Jeong last_name: Rhee - first_name: Nils full_name: Brose, Nils last_name: Brose citation: ama: Hammer M, Krueger Burg D, Tuffy L, et al. Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism. Cell Reports. 2015;13(3):516-523. doi:10.1016/j.celrep.2015.09.011 apa: Hammer, M., Krueger Burg, D., Tuffy, L., Cooper, B., Taschenberger, H., Goswami, S., … Brose, N. (2015). Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2015.09.011 chicago: Hammer, Matthieu, Dilja Krueger Burg, Liam Tuffy, Benjamin Cooper, Holger Taschenberger, Sarit Goswami, Hannelore Ehrenreich, et al. “Perturbed Hippocampal Synaptic Inhibition and γ-Oscillations in a Neuroligin-4 Knockout Mouse Model of Autism.” Cell Reports. Cell Press, 2015. https://doi.org/10.1016/j.celrep.2015.09.011. ieee: M. Hammer et al., “Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism,” Cell Reports, vol. 13, no. 3. Cell Press, pp. 516–523, 2015. ista: Hammer M, Krueger Burg D, Tuffy L, Cooper B, Taschenberger H, Goswami S, Ehrenreich H, Jonas PM, Varoqueaux F, Rhee J, Brose N. 2015. Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism. Cell Reports. 13(3), 516–523. mla: Hammer, Matthieu, et al. “Perturbed Hippocampal Synaptic Inhibition and γ-Oscillations in a Neuroligin-4 Knockout Mouse Model of Autism.” Cell Reports, vol. 13, no. 3, Cell Press, 2015, pp. 516–23, doi:10.1016/j.celrep.2015.09.011. short: M. Hammer, D. Krueger Burg, L. Tuffy, B. Cooper, H. Taschenberger, S. Goswami, H. Ehrenreich, P.M. Jonas, F. Varoqueaux, J. Rhee, N. Brose, Cell Reports 13 (2015) 516–523. date_created: 2018-12-11T11:53:02Z date_published: 2015-10-20T00:00:00Z date_updated: 2021-01-12T06:52:01Z day: '20' ddc: - '570' department: - _id: PeJo doi: 10.1016/j.celrep.2015.09.011 file: - access_level: open_access checksum: 44d30fbb543774b076b4938bd36af9d7 content_type: application/pdf creator: system date_created: 2018-12-12T10:13:23Z date_updated: 2020-07-14T12:45:07Z file_id: '5005' file_name: IST-2016-470-v1+1_1-s2.0-S2211124715010220-main.pdf file_size: 2314406 relation: main_file file_date_updated: 2020-07-14T12:45:07Z has_accepted_license: '1' intvolume: ' 13' issue: '3' language: - iso: eng month: '10' oa: 1 oa_version: Published Version page: 516 - 523 publication: Cell Reports publication_status: published publisher: Cell Press publist_id: '5551' pubrep_id: '470' quality_controlled: '1' scopus_import: 1 status: public title: Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 13 year: '2015' ... --- _id: '1614' abstract: - lang: eng text: 'GABAergic perisoma-inhibiting fast-spiking interneurons (PIIs) effectively control the activity of large neuron populations by their wide axonal arborizations. It is generally assumed that the output of one PII to its target cells is strong and rapid. Here, we show that, unexpectedly, both strength and time course of PII-mediated perisomatic inhibition change with distance between synaptically connected partners in the rodent hippocampus. Synaptic signals become weaker due to lower contact numbers and decay more slowly with distance, very likely resulting from changes in GABAA receptor subunit composition. When distance-dependent synaptic inhibition is introduced to a rhythmically active neuronal network model, randomly driven principal cell assemblies are strongly synchronized by the PIIs, leading to higher precision in principal cell spike times than in a network with uniform synaptic inhibition. ' author: - first_name: Michael full_name: Strüber, Michael last_name: Strüber - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 - first_name: Marlene full_name: Bartos, Marlene last_name: Bartos citation: ama: Strüber M, Jonas PM, Bartos M. Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells. PNAS. 2015;112(4):1220-1225. doi:10.1073/pnas.1412996112 apa: Strüber, M., Jonas, P. M., & Bartos, M. (2015). Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1412996112 chicago: Strüber, Michael, Peter M Jonas, and Marlene Bartos. “Strength and Duration of Perisomatic GABAergic Inhibition Depend on Distance between Synaptically Connected Cells.” PNAS. National Academy of Sciences, 2015. https://doi.org/10.1073/pnas.1412996112. ieee: M. Strüber, P. M. Jonas, and M. Bartos, “Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells,” PNAS, vol. 112, no. 4. National Academy of Sciences, pp. 1220–1225, 2015. ista: Strüber M, Jonas PM, Bartos M. 2015. Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells. PNAS. 112(4), 1220–1225. mla: Strüber, Michael, et al. “Strength and Duration of Perisomatic GABAergic Inhibition Depend on Distance between Synaptically Connected Cells.” PNAS, vol. 112, no. 4, National Academy of Sciences, 2015, pp. 1220–25, doi:10.1073/pnas.1412996112. short: M. Strüber, P.M. Jonas, M. Bartos, PNAS 112 (2015) 1220–1225. date_created: 2018-12-11T11:53:02Z date_published: 2015-01-27T00:00:00Z date_updated: 2021-01-12T06:52:01Z day: '27' ddc: - '570' department: - _id: PeJo doi: 10.1073/pnas.1412996112 ec_funded: 1 external_id: pmid: - '25583495' file: - access_level: open_access checksum: 6703309a1f58493cf5a704211fb6ebed content_type: application/pdf creator: dernst date_created: 2019-01-17T07:52:40Z date_updated: 2020-07-14T12:45:07Z file_id: '5838' file_name: 2015_PNAS_Strueber.pdf file_size: 1280860 relation: main_file file_date_updated: 2020-07-14T12:45:07Z has_accepted_license: '1' intvolume: ' 112' issue: '4' language: - iso: eng month: '01' oa: 1 oa_version: Published Version page: 1220 - 1225 pmid: 1 project: - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons publication: PNAS publication_status: published publisher: National Academy of Sciences publist_id: '5552' quality_controlled: '1' scopus_import: 1 status: public title: Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 112 year: '2015' ... --- _id: '1845' abstract: - lang: eng text: Based on extrapolation from excitatory synapses, it is often assumed that depletion of the releasable pool of synaptic vesicles is the main factor underlying depression at inhibitory synapses. In this issue of Neuron, using subcellular patch-clamp recording from inhibitory presynaptic terminals, Kawaguchi and Sakaba (2015) show that at Purkinje cell-deep cerebellar nuclei neuron synapses, changes in presynaptic action potential waveform substantially contribute to synaptic depression. Based on extrapolation from excitatory synapses, it is often assumed that depletion of the releasable pool of synaptic vesicles is the main factor underlying depression at inhibitory synapses. In this issue of Neuron, using subcellular patch-clamp recording from inhibitory presynaptic terminals, Kawaguchi and Sakaba (2015) show that at Purkinje cell-deep cerebellar nuclei neuron synapses, changes in presynaptic action potential waveform substantially contribute to synaptic depression. article_processing_charge: No author: - first_name: David H full_name: Vandael, David H id: 3AE48E0A-F248-11E8-B48F-1D18A9856A87 last_name: Vandael orcid: 0000-0001-7577-1676 - first_name: 'Claudia ' full_name: 'Espinoza Martinez, Claudia ' id: 31FFEE2E-F248-11E8-B48F-1D18A9856A87 last_name: Espinoza Martinez orcid: 0000-0003-4710-2082 - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Vandael DH, Espinoza Martinez C, Jonas PM. Excitement about inhibitory presynaptic terminals. Neuron. 2015;85(6):1149-1151. doi:10.1016/j.neuron.2015.03.006 apa: Vandael, D. H., Espinoza Martinez, C., & Jonas, P. M. (2015). Excitement about inhibitory presynaptic terminals. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2015.03.006 chicago: Vandael, David H, Claudia Espinoza Martinez, and Peter M Jonas. “Excitement about Inhibitory Presynaptic Terminals.” Neuron. Elsevier, 2015. https://doi.org/10.1016/j.neuron.2015.03.006. ieee: D. H. Vandael, C. Espinoza Martinez, and P. M. Jonas, “Excitement about inhibitory presynaptic terminals,” Neuron, vol. 85, no. 6. Elsevier, pp. 1149–1151, 2015. ista: Vandael DH, Espinoza Martinez C, Jonas PM. 2015. Excitement about inhibitory presynaptic terminals. Neuron. 85(6), 1149–1151. mla: Vandael, David H., et al. “Excitement about Inhibitory Presynaptic Terminals.” Neuron, vol. 85, no. 6, Elsevier, 2015, pp. 1149–51, doi:10.1016/j.neuron.2015.03.006. short: D.H. Vandael, C. Espinoza Martinez, P.M. Jonas, Neuron 85 (2015) 1149–1151. date_created: 2018-12-11T11:54:19Z date_published: 2015-03-18T00:00:00Z date_updated: 2021-10-08T09:07:34Z day: '18' ddc: - '570' department: - _id: PeJo doi: 10.1016/j.neuron.2015.03.006 file: - access_level: open_access checksum: d1808550e376a0eca2a950fda017cfa6 content_type: application/pdf creator: system date_created: 2018-12-12T10:16:07Z date_updated: 2020-07-14T12:45:19Z file_id: '5192' file_name: IST-2017-822-v1+1_Perspective_Fig__Final.pdf file_size: 411832 relation: main_file - access_level: open_access checksum: a279f4ae61e6c8f33d68f69a0d02097d content_type: application/pdf creator: system date_created: 2018-12-12T10:16:07Z date_updated: 2020-07-14T12:45:19Z file_id: '5193' file_name: IST-2017-822-v1+2_Perspective_Final2.pdf file_size: 100769 relation: main_file file_date_updated: 2020-07-14T12:45:19Z has_accepted_license: '1' intvolume: ' 85' issue: '6' language: - iso: eng month: '03' oa: 1 oa_version: Published Version page: 1149 - 1151 publication: Neuron publication_status: published publisher: Elsevier publist_id: '5256' pubrep_id: '822' quality_controlled: '1' scopus_import: '1' status: public title: Excitement about inhibitory presynaptic terminals tmp: image: /images/cc_by_nc.png legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) short: CC BY-NC (4.0) type: journal_article user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9 volume: 85 year: '2015' ... --- _id: '1834' abstract: - lang: eng text: Huge body of evidences demonstrated that volatile anesthetics affect the hippocampal neurogenesis and neurocognitive functions, and most of them showed impairment at anesthetic dose. Here, we investigated the effect of low dose (1.8%) sevoflurane on hippocampal neurogenesis and dentate gyrus-dependent learning. Neonatal rats at postnatal day 4 to 6 (P4-6) were treated with 1.8% sevoflurane for 6 hours. Neurogenesis was quantified by bromodeoxyuridine labeling and electrophysiology recording. Four and seven weeks after treatment, the Morris water maze and contextual-fear discrimination learning tests were performed to determine the influence on spatial learning and pattern separation. A 6-hour treatment with 1.8% sevoflurane promoted hippocampal neurogenesis and increased the survival of newborn cells and the proportion of immature granular cells in the dentate gyrus of neonatal rats. Sevoflurane-treated rats performed better during the training days of the Morris water maze test and in contextual-fear discrimination learning test. These results suggest that a subanesthetic dose of sevoflurane promotes hippocampal neurogenesis in neonatal rats and facilitates their performance in dentate gyrus-dependent learning tasks. article_processing_charge: No article_type: original author: - first_name: Chong full_name: Chen, Chong id: 3DFD581A-F248-11E8-B48F-1D18A9856A87 last_name: Chen - first_name: Chao full_name: Wang, Chao last_name: Wang - first_name: Xuan full_name: Zhao, Xuan last_name: Zhao - first_name: Tao full_name: Zhou, Tao last_name: Zhou - first_name: Dao full_name: Xu, Dao last_name: Xu - first_name: Zhi full_name: Wang, Zhi last_name: Wang - first_name: Ying full_name: Wang, Ying last_name: Wang citation: ama: Chen C, Wang C, Zhao X, et al. Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats. ASN Neuro. 2015;7(2). doi:10.1177/1759091415575845 apa: Chen, C., Wang, C., Zhao, X., Zhou, T., Xu, D., Wang, Z., & Wang, Y. (2015). Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats. ASN Neuro. SAGE Publications. https://doi.org/10.1177/1759091415575845 chicago: Chen, Chong, Chao Wang, Xuan Zhao, Tao Zhou, Dao Xu, Zhi Wang, and Ying Wang. “Low-Dose Sevoflurane Promoteshippocampal Neurogenesis and Facilitates the Development of Dentate Gyrus-Dependent Learning in Neonatal Rats.” ASN Neuro. SAGE Publications, 2015. https://doi.org/10.1177/1759091415575845. ieee: C. Chen et al., “Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats,” ASN Neuro, vol. 7, no. 2. SAGE Publications, 2015. ista: Chen C, Wang C, Zhao X, Zhou T, Xu D, Wang Z, Wang Y. 2015. Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats. ASN Neuro. 7(2). mla: Chen, Chong, et al. “Low-Dose Sevoflurane Promoteshippocampal Neurogenesis and Facilitates the Development of Dentate Gyrus-Dependent Learning in Neonatal Rats.” ASN Neuro, vol. 7, no. 2, SAGE Publications, 2015, doi:10.1177/1759091415575845. short: C. Chen, C. Wang, X. Zhao, T. Zhou, D. Xu, Z. Wang, Y. Wang, ASN Neuro 7 (2015). date_created: 2018-12-11T11:54:16Z date_published: 2015-04-13T00:00:00Z date_updated: 2023-10-18T06:47:30Z day: '13' ddc: - '570' department: - _id: PeJo doi: 10.1177/1759091415575845 file: - access_level: open_access checksum: 53e16bd3fc2ae2c0d7de9164626c37aa content_type: application/pdf creator: system date_created: 2018-12-12T10:14:08Z date_updated: 2020-07-14T12:45:18Z file_id: '5057' file_name: IST-2016-456-v1+1_ASN_Neuro-2015-Chen-.pdf file_size: 1146814 relation: main_file file_date_updated: 2020-07-14T12:45:18Z has_accepted_license: '1' intvolume: ' 7' issue: '2' language: - iso: eng license: https://creativecommons.org/licenses/by/3.0/ month: '04' oa: 1 oa_version: Published Version publication: ASN Neuro publication_status: published publisher: SAGE Publications publist_id: '5269' pubrep_id: '456' quality_controlled: '1' scopus_import: '1' status: public title: Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/3.0/legalcode name: Creative Commons Attribution 3.0 Unported (CC BY 3.0) short: CC BY (3.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 7 year: '2015' ... --- _id: '1890' abstract: - lang: eng text: To search for a target in a complex environment is an everyday behavior that ends with finding the target. When we search for two identical targets, however, we must continue the search after finding the first target and memorize its location. We used fixation-related potentials to investigate the neural correlates of different stages of the search, that is, before and after finding the first target. Having found the first target influenced subsequent distractor processing. Compared to distractor fixations before the first target fixation, a negative shift was observed for three subsequent distractor fixations. These results suggest that processing a target in continued search modulates the brain's response, either transiently by reflecting temporary working memory processes or permanently by reflecting working memory retention. acknowledgement: 'Funded by Austrian Science Fund (FWF) Grant Number: P 22189-B18; European Union within the 6th Framework Programme Grant Number: 517590; State government of Styria Grant Number: PN 4055' author: - first_name: Christof full_name: Körner, Christof last_name: Körner - first_name: Verena full_name: Braunstein, Verena last_name: Braunstein - first_name: Matthias full_name: Stangl, Matthias last_name: Stangl - first_name: Alois full_name: Schlögl, Alois id: 45BF87EE-F248-11E8-B48F-1D18A9856A87 last_name: Schlögl orcid: 0000-0002-5621-8100 - first_name: Christa full_name: Neuper, Christa last_name: Neuper - first_name: Anja full_name: Ischebeck, Anja last_name: Ischebeck citation: ama: 'Körner C, Braunstein V, Stangl M, Schlögl A, Neuper C, Ischebeck A. Sequential effects in continued visual search: Using fixation-related potentials to compare distractor processing before and after target detection. Psychophysiology. 2014;51(4):385-395. doi:10.1111/psyp.12062' apa: 'Körner, C., Braunstein, V., Stangl, M., Schlögl, A., Neuper, C., & Ischebeck, A. (2014). Sequential effects in continued visual search: Using fixation-related potentials to compare distractor processing before and after target detection. Psychophysiology. Wiley-Blackwell. https://doi.org/10.1111/psyp.12062' chicago: 'Körner, Christof, Verena Braunstein, Matthias Stangl, Alois Schlögl, Christa Neuper, and Anja Ischebeck. “Sequential Effects in Continued Visual Search: Using Fixation-Related Potentials to Compare Distractor Processing before and after Target Detection.” Psychophysiology. Wiley-Blackwell, 2014. https://doi.org/10.1111/psyp.12062.' ieee: 'C. Körner, V. Braunstein, M. Stangl, A. Schlögl, C. Neuper, and A. Ischebeck, “Sequential effects in continued visual search: Using fixation-related potentials to compare distractor processing before and after target detection,” Psychophysiology, vol. 51, no. 4. Wiley-Blackwell, pp. 385–395, 2014.' ista: 'Körner C, Braunstein V, Stangl M, Schlögl A, Neuper C, Ischebeck A. 2014. Sequential effects in continued visual search: Using fixation-related potentials to compare distractor processing before and after target detection. Psychophysiology. 51(4), 385–395.' mla: 'Körner, Christof, et al. “Sequential Effects in Continued Visual Search: Using Fixation-Related Potentials to Compare Distractor Processing before and after Target Detection.” Psychophysiology, vol. 51, no. 4, Wiley-Blackwell, 2014, pp. 385–95, doi:10.1111/psyp.12062.' short: C. Körner, V. Braunstein, M. Stangl, A. Schlögl, C. Neuper, A. Ischebeck, Psychophysiology 51 (2014) 385–395. date_created: 2018-12-11T11:54:34Z date_published: 2014-02-11T00:00:00Z date_updated: 2021-01-12T06:53:52Z day: '11' ddc: - '000' department: - _id: ScienComp - _id: PeJo doi: 10.1111/psyp.12062 file: - access_level: open_access checksum: 4255b6185e774acce1d99f8e195c564d content_type: application/pdf creator: system date_created: 2018-12-12T10:16:44Z date_updated: 2020-07-14T12:45:20Z file_id: '5233' file_name: IST-2016-442-v1+1_K-rner_et_al-2014-Psychophysiology.pdf file_size: 543243 relation: main_file file_date_updated: 2020-07-14T12:45:20Z has_accepted_license: '1' intvolume: ' 51' issue: '4' language: - iso: eng month: '02' oa: 1 oa_version: Published Version page: 385 - 395 publication: Psychophysiology publication_status: published publisher: Wiley-Blackwell publist_id: '5205' pubrep_id: '442' scopus_import: 1 status: public title: 'Sequential effects in continued visual search: Using fixation-related potentials to compare distractor processing before and after target detection' tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 51 year: '2014' ... --- _id: '2002' abstract: - lang: eng text: Oriens-lacunosum moleculare (O-LM) interneurons in the CA1 region of the hippocampus play a key role in feedback inhibition and in the control of network activity. However, how these cells are efficiently activated in the network remains unclear. To address this question, I performed recordings from CA1 pyramidal neuron axons, the presynaptic fibers that provide feedback innervation of these interneurons. Two forms of axonal action potential (AP) modulation were identified. First, repetitive stimulation resulted in activity-dependent AP broadening. Broadening showed fast onset, with marked changes in AP shape following a single AP. Second, tonic depolarization in CA1 pyramidal neuron somata induced AP broadening in the axon, and depolarization-induced broadening summated with activity-dependent broadening. Outsideout patch recordings from CA1 pyramidal neuron axons revealed a high density of a-dendrotoxin (α-DTX)-sensitive, inactivating K+ channels, suggesting that K+ channel inactivation mechanistically contributes to AP broadening. To examine the functional consequences of axonal AP modulation for synaptic transmission, I performed paired recordings between synaptically connected CA1 pyramidal neurons and O-LM interneurons. CA1 pyramidal neuron-O-LM interneuron excitatory postsynaptic currents (EPSCs) showed facilitation during both repetitive stimulation and tonic depolarization of the presynaptic neuron. Both effects were mimicked and occluded by α-DTX, suggesting that they were mediated by K+ channel inactivation. Therefore, axonal AP modulation can greatly facilitate the activation of O-LM interneurons. In conclusion, modulation of AP shape in CA1 pyramidal neuron axons substantially enhances the efficacy of principal neuron-interneuron synapses, promoting the activation of O-LM interneurons in recurrent inhibitory microcircuits. article_number: '0113124' author: - first_name: Sooyun full_name: Kim, Sooyun id: 394AB1C8-F248-11E8-B48F-1D18A9856A87 last_name: Kim citation: ama: Kim S. Action potential modulation in CA1 pyramidal neuron axons facilitates OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus. PLoS One. 2014;9(11). doi:10.1371/journal.pone.0113124 apa: Kim, S. (2014). Action potential modulation in CA1 pyramidal neuron axons facilitates OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0113124 chicago: Kim, Sooyun. “Action Potential Modulation in CA1 Pyramidal Neuron Axons Facilitates OLM Interneuron Activation in Recurrent Inhibitory Microcircuits of Rat Hippocampus.” PLoS One. Public Library of Science, 2014. https://doi.org/10.1371/journal.pone.0113124. ieee: S. Kim, “Action potential modulation in CA1 pyramidal neuron axons facilitates OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus,” PLoS One, vol. 9, no. 11. Public Library of Science, 2014. ista: Kim S. 2014. Action potential modulation in CA1 pyramidal neuron axons facilitates OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus. PLoS One. 9(11), 0113124. mla: Kim, Sooyun. “Action Potential Modulation in CA1 Pyramidal Neuron Axons Facilitates OLM Interneuron Activation in Recurrent Inhibitory Microcircuits of Rat Hippocampus.” PLoS One, vol. 9, no. 11, 0113124, Public Library of Science, 2014, doi:10.1371/journal.pone.0113124. short: S. Kim, PLoS One 9 (2014). date_created: 2018-12-11T11:55:09Z date_published: 2014-11-19T00:00:00Z date_updated: 2021-01-12T06:54:39Z day: '19' ddc: - '570' department: - _id: PeJo doi: 10.1371/journal.pone.0113124 ec_funded: 1 file: - access_level: open_access checksum: 85e4f4ea144f827272aaf376b2830564 content_type: application/pdf creator: system date_created: 2018-12-12T10:14:52Z date_updated: 2020-07-14T12:45:24Z file_id: '5107' file_name: IST-2016-434-v1+1_journal.pone.0113124.pdf file_size: 5179993 relation: main_file file_date_updated: 2020-07-14T12:45:24Z has_accepted_license: '1' intvolume: ' 9' issue: '11' language: - iso: eng license: https://creativecommons.org/licenses/by-sa/4.0/ month: '11' oa: 1 oa_version: Published Version project: - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons publication: PLoS One publication_status: published publisher: Public Library of Science publist_id: '5074' pubrep_id: '434' quality_controlled: '1' scopus_import: 1 status: public title: Action potential modulation in CA1 pyramidal neuron axons facilitates OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus tmp: image: /images/cc_by_sa.png legal_code_url: https://creativecommons.org/licenses/by-sa/4.0/legalcode name: Creative Commons Attribution-ShareAlike 4.0 International Public License (CC BY-SA 4.0) short: CC BY-SA (4.0) type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 9 year: '2014' ... --- _id: '2031' abstract: - lang: eng text: A puzzling property of synaptic transmission, originally established at the neuromuscular junction, is that the time course of transmitter release is independent of the extracellular Ca2+ concentration ([Ca2+]o), whereas the rate of release is highly [Ca2+]o-dependent. Here, we examine the time course of release at inhibitory basket cell-Purkinje cell synapses and show that it is independent of [Ca2+]o. Modeling of Ca2+-dependent transmitter release suggests that the invariant time course of release critically depends on tight coupling between Ca2+ channels and release sensors. Experiments with exogenous Ca2+ chelators reveal that channel-sensor coupling at basket cell-Purkinje cell synapses is very tight, with a mean distance of 10–20 nm. Thus, tight channel-sensor coupling provides a mechanistic explanation for the apparent [Ca2+]o independence of the time course of release. author: - first_name: Itaru full_name: Arai, Itaru id: 32A73F6C-F248-11E8-B48F-1D18A9856A87 last_name: Arai - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Arai itaru, Jonas PM. Nanodomain coupling explains Ca^2+ independence of transmitter release time course at a fast central synapse. eLife. 2014;3. doi:10.7554/eLife.04057 apa: Arai, itaru, & Jonas, P. M. (2014). Nanodomain coupling explains Ca^2+ independence of transmitter release time course at a fast central synapse. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.04057 chicago: Arai, itaru, and Peter M Jonas. “Nanodomain Coupling Explains Ca^2+ Independence of Transmitter Release Time Course at a Fast Central Synapse.” ELife. eLife Sciences Publications, 2014. https://doi.org/10.7554/eLife.04057. ieee: itaru Arai and P. M. Jonas, “Nanodomain coupling explains Ca^2+ independence of transmitter release time course at a fast central synapse,” eLife, vol. 3. eLife Sciences Publications, 2014. ista: Arai itaru, Jonas PM. 2014. Nanodomain coupling explains Ca^2+ independence of transmitter release time course at a fast central synapse. eLife. 3. mla: Arai, itaru, and Peter M. Jonas. “Nanodomain Coupling Explains Ca^2+ Independence of Transmitter Release Time Course at a Fast Central Synapse.” ELife, vol. 3, eLife Sciences Publications, 2014, doi:10.7554/eLife.04057. short: itaru Arai, P.M. Jonas, ELife 3 (2014). date_created: 2018-12-11T11:55:19Z date_published: 2014-12-09T00:00:00Z date_updated: 2021-01-12T06:54:51Z day: '09' ddc: - '570' department: - _id: PeJo doi: 10.7554/eLife.04057 ec_funded: 1 file: - access_level: open_access checksum: c240f915450d4ebe8f95043a2a8c7b1a content_type: application/pdf creator: system date_created: 2018-12-12T10:14:41Z date_updated: 2020-07-14T12:45:26Z file_id: '5094' file_name: IST-2016-421-v1+1_e04057.full.pdf file_size: 2239563 relation: main_file file_date_updated: 2020-07-14T12:45:26Z has_accepted_license: '1' intvolume: ' 3' language: - iso: eng month: '12' oa: 1 oa_version: Submitted Version project: - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons publication: eLife publication_status: published publisher: eLife Sciences Publications publist_id: '5041' pubrep_id: '421' quality_controlled: '1' scopus_import: 1 status: public title: Nanodomain coupling explains Ca^2+ independence of transmitter release time course at a fast central synapse type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 3 year: '2014' ... --- _id: '2041' abstract: - lang: eng text: The hippocampus mediates several higher brain functions, such as learning, memory, and spatial coding. The input region of the hippocampus, the dentate gyrus, plays a critical role in these processes. Several lines of evidence suggest that the dentate gyrus acts as a preprocessor of incoming information, preparing it for subsequent processing in CA3. For example, the dentate gyrus converts input from the entorhinal cortex, where cells have multiple spatial fields, into the spatially more specific place cell activity characteristic of the CA3 region. Furthermore, the dentate gyrus is involved in pattern separation, transforming relatively similar input patterns into substantially different output patterns. Finally, the dentate gyrus produces a very sparse coding scheme in which only a very small fraction of neurons are active at any one time. article_number: 2p author: - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 - first_name: John full_name: Lisman, John last_name: Lisman citation: ama: Jonas PM, Lisman J. Structure, function and plasticity of hippocampal dentate gyrus microcircuits. Frontiers in Neural Circuits. 2014;8. doi:10.3389/fncir.2014.00107 apa: Jonas, P. M., & Lisman, J. (2014). Structure, function and plasticity of hippocampal dentate gyrus microcircuits. Frontiers in Neural Circuits. Frontiers Research Foundation. https://doi.org/10.3389/fncir.2014.00107 chicago: Jonas, Peter M, and John Lisman. “Structure, Function and Plasticity of Hippocampal Dentate Gyrus Microcircuits.” Frontiers in Neural Circuits. Frontiers Research Foundation, 2014. https://doi.org/10.3389/fncir.2014.00107. ieee: P. M. Jonas and J. Lisman, “Structure, function and plasticity of hippocampal dentate gyrus microcircuits,” Frontiers in Neural Circuits, vol. 8. Frontiers Research Foundation, 2014. ista: Jonas PM, Lisman J. 2014. Structure, function and plasticity of hippocampal dentate gyrus microcircuits. Frontiers in Neural Circuits. 8, 2p. mla: Jonas, Peter M., and John Lisman. “Structure, Function and Plasticity of Hippocampal Dentate Gyrus Microcircuits.” Frontiers in Neural Circuits, vol. 8, 2p, Frontiers Research Foundation, 2014, doi:10.3389/fncir.2014.00107. short: P.M. Jonas, J. Lisman, Frontiers in Neural Circuits 8 (2014). date_created: 2018-12-11T11:55:22Z date_published: 2014-09-10T00:00:00Z date_updated: 2021-01-12T06:54:55Z day: '10' ddc: - '570' department: - _id: PeJo doi: 10.3389/fncir.2014.00107 file: - access_level: open_access checksum: 3ca57b164045523f876407e9f13a9fb8 content_type: application/pdf creator: system date_created: 2018-12-12T10:17:38Z date_updated: 2020-07-14T12:45:26Z file_id: '5294' file_name: IST-2016-424-v1+1_fncir-08-00107.pdf file_size: 201110 relation: main_file file_date_updated: 2020-07-14T12:45:26Z has_accepted_license: '1' intvolume: ' 8' language: - iso: eng month: '09' oa: 1 oa_version: Published Version publication: Frontiers in Neural Circuits publication_status: published publisher: Frontiers Research Foundation publist_id: '5010' pubrep_id: '424' quality_controlled: '1' scopus_import: 1 status: public title: Structure, function and plasticity of hippocampal dentate gyrus microcircuits tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 8 year: '2014' ... --- _id: '2062' abstract: - lang: eng text: The success story of fast-spiking, parvalbumin-positive (PV+) GABAergic interneurons (GABA, γ-aminobutyric acid) in the mammalian central nervous system is noteworthy. In 1995, the properties of these interneurons were completely unknown. Twenty years later, thanks to the massive use of subcellular patch-clamp techniques, simultaneous multiple-cell recording, optogenetics, in vivo measurements, and computational approaches, our knowledge about PV+ interneurons became more extensive than for several types of pyramidal neurons. These findings have implications beyond the “small world” of basic research on GABAergic cells. For example, the results provide a first proof of principle that neuroscientists might be able to close the gaps between the molecular, cellular, network, and behavioral levels, representing one of the main challenges at the present time. Furthermore, the results may form the basis for PV+ interneurons as therapeutic targets for brain disease in the future. However, much needs to be learned about the basic function of these interneurons before clinical neuroscientists will be able to use PV+ interneurons for therapeutic purposes. article_number: '1255263' author: - first_name: Hua full_name: Hu, Hua id: 4AC0145C-F248-11E8-B48F-1D18A9856A87 last_name: Hu - first_name: Jian full_name: Gan, Jian id: 3614E438-F248-11E8-B48F-1D18A9856A87 last_name: Gan - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: 'Hu H, Gan J, Jonas PM. Fast-spiking parvalbumin^+ GABAergic interneurons: From cellular design to microcircuit function. Science. 2014;345(6196). doi:10.1126/science.1255263' apa: 'Hu, H., Gan, J., & Jonas, P. M. (2014). Fast-spiking parvalbumin^+ GABAergic interneurons: From cellular design to microcircuit function. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.1255263' chicago: 'Hu, Hua, Jian Gan, and Peter M Jonas. “Fast-Spiking Parvalbumin^+ GABAergic Interneurons: From Cellular Design to Microcircuit Function.” Science. American Association for the Advancement of Science, 2014. https://doi.org/10.1126/science.1255263.' ieee: 'H. Hu, J. Gan, and P. M. Jonas, “Fast-spiking parvalbumin^+ GABAergic interneurons: From cellular design to microcircuit function,” Science, vol. 345, no. 6196. American Association for the Advancement of Science, 2014.' ista: 'Hu H, Gan J, Jonas PM. 2014. Fast-spiking parvalbumin^+ GABAergic interneurons: From cellular design to microcircuit function. Science. 345(6196), 1255263.' mla: 'Hu, Hua, et al. “Fast-Spiking Parvalbumin^+ GABAergic Interneurons: From Cellular Design to Microcircuit Function.” Science, vol. 345, no. 6196, 1255263, American Association for the Advancement of Science, 2014, doi:10.1126/science.1255263.' short: H. Hu, J. Gan, P.M. Jonas, Science 345 (2014). date_created: 2018-12-11T11:55:29Z date_published: 2014-08-01T00:00:00Z date_updated: 2021-01-12T06:55:03Z day: '01' ddc: - '570' department: - _id: PeJo doi: 10.1126/science.1255263 ec_funded: 1 file: - access_level: open_access checksum: a0036a589037d37e86364fa25cc0a82f content_type: application/pdf creator: system date_created: 2018-12-12T10:16:00Z date_updated: 2020-07-14T12:45:27Z file_id: '5185' file_name: IST-2017-821-v1+1_1255263JonasPVReviewTextR_Final.pdf file_size: 215514 relation: main_file - access_level: open_access checksum: e1f57d2713725449cb898fdcb8ef47b8 content_type: application/pdf creator: system date_created: 2018-12-12T10:16:01Z date_updated: 2020-07-14T12:45:27Z file_id: '5186' file_name: IST-2017-821-v1+2_1255263JonasPVReviewFigures_Final.pdf file_size: 1732723 relation: main_file file_date_updated: 2020-07-14T12:45:27Z has_accepted_license: '1' intvolume: ' 345' issue: '6196' language: - iso: eng month: '08' oa: 1 oa_version: Submitted Version project: - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons publication: Science publication_status: published publisher: American Association for the Advancement of Science publist_id: '4984' pubrep_id: '821' quality_controlled: '1' scopus_import: 1 status: public title: 'Fast-spiking parvalbumin^+ GABAergic interneurons: From cellular design to microcircuit function' type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 345 year: '2014' ... --- _id: '2164' abstract: - lang: eng text: 'Neuronal ectopia, such as granule cell dispersion (GCD) in temporal lobe epilepsy (TLE), has been assumed to result from a migration defect during development. Indeed, recent studies reported that aberrant migration of neonatal-generated dentate granule cells (GCs) increased the risk to develop epilepsy later in life. On the contrary, in the present study, we show that fully differentiated GCs become motile following the induction of epileptiform activity, resulting in GCD. Hippocampal slice cultures from transgenic mice expressing green fluorescent protein in differentiated, but not in newly generated GCs, were incubated with the glutamate receptor agonist kainate (KA), which induced GC burst activity and GCD. Using real-time microscopy, we observed that KA-exposed, differentiated GCs translocated their cell bodies and changed their dendritic organization. As found in human TLE, KA application was associated with decreased expression of the extracellular matrix protein Reelin, particularly in hilar interneurons. Together these findings suggest that KA-induced motility of differentiated GCs contributes to the development of GCD and establish slice cultures as a model to study neuronal changes induced by epileptiform activity. ' author: - first_name: Xuejun full_name: Chai, Xuejun last_name: Chai - first_name: Gert full_name: Münzner, Gert last_name: Münzner - first_name: Shanting full_name: Zhao, Shanting last_name: Zhao - first_name: Stefanie full_name: Tinnes, Stefanie last_name: Tinnes - first_name: Janina full_name: Kowalski, Janina id: 3F3CA136-F248-11E8-B48F-1D18A9856A87 last_name: Kowalski - first_name: Ute full_name: Häussler, Ute last_name: Häussler - first_name: Christina full_name: Young, Christina last_name: Young - first_name: Carola full_name: Haas, Carola last_name: Haas - first_name: Michael full_name: Frotscher, Michael last_name: Frotscher citation: ama: Chai X, Münzner G, Zhao S, et al. Epilepsy-induced motility of differentiated neurons. Cerebral Cortex. 2014;24(8):2130-2140. doi:10.1093/cercor/bht067 apa: Chai, X., Münzner, G., Zhao, S., Tinnes, S., Kowalski, J., Häussler, U., … Frotscher, M. (2014). Epilepsy-induced motility of differentiated neurons. Cerebral Cortex. Oxford University Press. https://doi.org/10.1093/cercor/bht067 chicago: Chai, Xuejun, Gert Münzner, Shanting Zhao, Stefanie Tinnes, Janina Kowalski, Ute Häussler, Christina Young, Carola Haas, and Michael Frotscher. “Epilepsy-Induced Motility of Differentiated Neurons.” Cerebral Cortex. Oxford University Press, 2014. https://doi.org/10.1093/cercor/bht067. ieee: X. Chai et al., “Epilepsy-induced motility of differentiated neurons,” Cerebral Cortex, vol. 24, no. 8. Oxford University Press, pp. 2130–2140, 2014. ista: Chai X, Münzner G, Zhao S, Tinnes S, Kowalski J, Häussler U, Young C, Haas C, Frotscher M. 2014. Epilepsy-induced motility of differentiated neurons. Cerebral Cortex. 24(8), 2130–2140. mla: Chai, Xuejun, et al. “Epilepsy-Induced Motility of Differentiated Neurons.” Cerebral Cortex, vol. 24, no. 8, Oxford University Press, 2014, pp. 2130–40, doi:10.1093/cercor/bht067. short: X. Chai, G. Münzner, S. Zhao, S. Tinnes, J. Kowalski, U. Häussler, C. Young, C. Haas, M. Frotscher, Cerebral Cortex 24 (2014) 2130–2140. date_created: 2018-12-11T11:56:04Z date_published: 2014-08-01T00:00:00Z date_updated: 2021-01-12T06:55:43Z day: '01' department: - _id: PeJo doi: 10.1093/cercor/bht067 intvolume: ' 24' issue: '8' language: - iso: eng month: '08' oa_version: None page: 2130 - 2140 publication: Cerebral Cortex publication_status: published publisher: Oxford University Press publist_id: '4820' quality_controlled: '1' scopus_import: 1 status: public title: Epilepsy-induced motility of differentiated neurons type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 24 year: '2014' ... --- _id: '2176' abstract: - lang: eng text: Electron microscopy (EM) allows for the simultaneous visualization of all tissue components at high resolution. However, the extent to which conventional aldehyde fixation and ethanol dehydration of the tissue alter the fine structure of cells and organelles, thereby preventing detection of subtle structural changes induced by an experiment, has remained an issue. Attempts have been made to rapidly freeze tissue to preserve native ultrastructure. Shock-freezing of living tissue under high pressure (high-pressure freezing, HPF) followed by cryosubstitution of the tissue water avoids aldehyde fixation and dehydration in ethanol; the tissue water is immobilized in â ̂1/450 ms, and a close-to-native fine structure of cells, organelles and molecules is preserved. Here we describe a protocol for HPF that is useful to monitor ultrastructural changes associated with functional changes at synapses in the brain but can be applied to many other tissues as well. The procedure requires a high-pressure freezer and takes a minimum of 7 d but can be paused at several points. author: - first_name: Daniel full_name: Studer, Daniel last_name: Studer - first_name: Shanting full_name: Zhao, Shanting last_name: Zhao - first_name: Xuejun full_name: Chai, Xuejun last_name: Chai - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 - first_name: Werner full_name: Graber, Werner last_name: Graber - first_name: Sigrun full_name: Nestel, Sigrun last_name: Nestel - first_name: Michael full_name: Frotscher, Michael last_name: Frotscher citation: ama: Studer D, Zhao S, Chai X, et al. Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue. Nature Protocols. 2014;9(6):1480-1495. doi:10.1038/nprot.2014.099 apa: Studer, D., Zhao, S., Chai, X., Jonas, P. M., Graber, W., Nestel, S., & Frotscher, M. (2014). Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue. Nature Protocols. Nature Publishing Group. https://doi.org/10.1038/nprot.2014.099 chicago: Studer, Daniel, Shanting Zhao, Xuejun Chai, Peter M Jonas, Werner Graber, Sigrun Nestel, and Michael Frotscher. “Capture of Activity-Induced Ultrastructural Changes at Synapses by High-Pressure Freezing of Brain Tissue.” Nature Protocols. Nature Publishing Group, 2014. https://doi.org/10.1038/nprot.2014.099. ieee: D. Studer et al., “Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue,” Nature Protocols, vol. 9, no. 6. Nature Publishing Group, pp. 1480–1495, 2014. ista: Studer D, Zhao S, Chai X, Jonas PM, Graber W, Nestel S, Frotscher M. 2014. Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue. Nature Protocols. 9(6), 1480–1495. mla: Studer, Daniel, et al. “Capture of Activity-Induced Ultrastructural Changes at Synapses by High-Pressure Freezing of Brain Tissue.” Nature Protocols, vol. 9, no. 6, Nature Publishing Group, 2014, pp. 1480–95, doi:10.1038/nprot.2014.099. short: D. Studer, S. Zhao, X. Chai, P.M. Jonas, W. Graber, S. Nestel, M. Frotscher, Nature Protocols 9 (2014) 1480–1495. date_created: 2018-12-11T11:56:09Z date_published: 2014-05-29T00:00:00Z date_updated: 2021-01-12T06:55:47Z day: '29' department: - _id: PeJo doi: 10.1038/nprot.2014.099 intvolume: ' 9' issue: '6' language: - iso: eng month: '05' oa_version: None page: 1480 - 1495 project: - _id: 25BDE9A4-B435-11E9-9278-68D0E5697425 grant_number: SFB-TR3-TP10B name: Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen publication: Nature Protocols publication_status: published publisher: Nature Publishing Group publist_id: '4807' quality_controlled: '1' scopus_import: 1 status: public title: Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 9 year: '2014' ... --- _id: '2230' abstract: - lang: eng text: Intracellular electrophysiological recordings provide crucial insights into elementary neuronal signals such as action potentials and synaptic currents. Analyzing and interpreting these signals is essential for a quantitative understanding of neuronal information processing, and requires both fast data visualization and ready access to complex analysis routines. To achieve this goal, we have developed Stimfit, a free software package for cellular neurophysiology with a Python scripting interface and a built-in Python shell. The program supports most standard file formats for cellular neurophysiology and other biomedical signals through the Biosig library. To quantify and interpret the activity of single neurons and communication between neurons, the program includes algorithms to characterize the kinetics of presynaptic action potentials and postsynaptic currents, estimate latencies between pre- and postsynaptic events, and detect spontaneously occurring events. We validate and benchmark these algorithms, give estimation errors, and provide sample use cases, showing that Stimfit represents an efficient, accessible and extensible way to accurately analyze and interpret neuronal signals. article_number: '16' author: - first_name: José full_name: Guzmán, José id: 30CC5506-F248-11E8-B48F-1D18A9856A87 last_name: Guzmán - first_name: Alois full_name: Schlögl, Alois id: 45BF87EE-F248-11E8-B48F-1D18A9856A87 last_name: Schlögl orcid: 0000-0002-5621-8100 - first_name: Christoph full_name: Schmidt Hieber, Christoph last_name: Schmidt Hieber citation: ama: 'Guzmán J, Schlögl A, Schmidt Hieber C. Stimfit: Quantifying electrophysiological data with Python. Frontiers in Neuroinformatics. 2014;8(FEB). doi:10.3389/fninf.2014.00016' apa: 'Guzmán, J., Schlögl, A., & Schmidt Hieber, C. (2014). Stimfit: Quantifying electrophysiological data with Python. Frontiers in Neuroinformatics. Frontiers Research Foundation. https://doi.org/10.3389/fninf.2014.00016' chicago: 'Guzmán, José, Alois Schlögl, and Christoph Schmidt Hieber. “Stimfit: Quantifying Electrophysiological Data with Python.” Frontiers in Neuroinformatics. Frontiers Research Foundation, 2014. https://doi.org/10.3389/fninf.2014.00016.' ieee: 'J. Guzmán, A. Schlögl, and C. Schmidt Hieber, “Stimfit: Quantifying electrophysiological data with Python,” Frontiers in Neuroinformatics, vol. 8, no. FEB. Frontiers Research Foundation, 2014.' ista: 'Guzmán J, Schlögl A, Schmidt Hieber C. 2014. Stimfit: Quantifying electrophysiological data with Python. Frontiers in Neuroinformatics. 8(FEB), 16.' mla: 'Guzmán, José, et al. “Stimfit: Quantifying Electrophysiological Data with Python.” Frontiers in Neuroinformatics, vol. 8, no. FEB, 16, Frontiers Research Foundation, 2014, doi:10.3389/fninf.2014.00016.' short: J. Guzmán, A. Schlögl, C. Schmidt Hieber, Frontiers in Neuroinformatics 8 (2014). date_created: 2018-12-11T11:56:27Z date_published: 2014-02-21T00:00:00Z date_updated: 2021-01-12T06:56:09Z day: '21' ddc: - '570' department: - _id: ScienComp - _id: PeJo doi: 10.3389/fninf.2014.00016 file: - access_level: open_access checksum: eeca00bba7232ff7d27db83321f6ea30 content_type: application/pdf creator: system date_created: 2018-12-12T10:12:17Z date_updated: 2020-07-14T12:45:34Z file_id: '4935' file_name: IST-2016-425-v1+1_fninf-08-00016.pdf file_size: 2883372 relation: main_file file_date_updated: 2020-07-14T12:45:34Z has_accepted_license: '1' intvolume: ' 8' issue: FEB language: - iso: eng month: '02' oa: 1 oa_version: Published Version publication: Frontiers in Neuroinformatics publication_identifier: issn: - '16625196' publication_status: published publisher: Frontiers Research Foundation publist_id: '4731' pubrep_id: '425' quality_controlled: '1' scopus_import: 1 status: public title: 'Stimfit: Quantifying electrophysiological data with Python' tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 8 year: '2014' ... --- _id: '2228' abstract: - lang: eng text: Fast-spiking, parvalbumin-expressing GABAergic interneurons, a large proportion of which are basket cells (BCs), have a key role in feedforward and feedback inhibition, gamma oscillations and complex information processing. For these functions, fast propagation of action potentials (APs) from the soma to the presynaptic terminals is important. However, the functional properties of interneuron axons remain elusive. We examined interneuron axons by confocally targeted subcellular patch-clamp recording in rat hippocampal slices. APs were initiated in the proximal axon ∼20 μm from the soma and propagated to the distal axon with high reliability and speed. Subcellular mapping revealed a stepwise increase of Na^+ conductance density from the soma to the proximal axon, followed by a further gradual increase in the distal axon. Active cable modeling and experiments with partial channel block revealed that low axonal Na^+ conductance density was sufficient for reliability, but high Na^+ density was necessary for both speed of propagation and fast-spiking AP phenotype. Our results suggest that a supercritical density of Na^+ channels compensates for the morphological properties of interneuron axons (small segmental diameter, extensive branching and high bouton density), ensuring fast AP propagation and high-frequency repetitive firing. author: - first_name: Hua full_name: Hu, Hua id: 4AC0145C-F248-11E8-B48F-1D18A9856A87 last_name: Hu - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Hu H, Jonas PM. A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons. Nature Neuroscience. 2014;17(5):686-693. doi:10.1038/nn.3678 apa: Hu, H., & Jonas, P. M. (2014). A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons. Nature Neuroscience. Nature Publishing Group. https://doi.org/10.1038/nn.3678 chicago: Hu, Hua, and Peter M Jonas. “A Supercritical Density of Na^+ Channels Ensures Fast Signaling in GABAergic Interneuron Axons.” Nature Neuroscience. Nature Publishing Group, 2014. https://doi.org/10.1038/nn.3678. ieee: H. Hu and P. M. Jonas, “A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons,” Nature Neuroscience, vol. 17, no. 5. Nature Publishing Group, pp. 686–693, 2014. ista: Hu H, Jonas PM. 2014. A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons. Nature Neuroscience. 17(5), 686–693. mla: Hu, Hua, and Peter M. Jonas. “A Supercritical Density of Na^+ Channels Ensures Fast Signaling in GABAergic Interneuron Axons.” Nature Neuroscience, vol. 17, no. 5, Nature Publishing Group, 2014, pp. 686–93, doi:10.1038/nn.3678. short: H. Hu, P.M. Jonas, Nature Neuroscience 17 (2014) 686–693. date_created: 2018-12-11T11:56:26Z date_published: 2014-03-23T00:00:00Z date_updated: 2021-01-12T06:56:08Z day: '23' department: - _id: PeJo doi: 10.1038/nn.3678 ec_funded: 1 intvolume: ' 17' issue: '5' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4286295/ month: '03' oa: 1 oa_version: Submitted Version page: 686-693 project: - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses publication: Nature Neuroscience publication_identifier: issn: - '10976256' publication_status: published publisher: Nature Publishing Group publist_id: '4733' quality_controlled: '1' scopus_import: 1 status: public title: A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 17 year: '2014' ... --- _id: '2229' abstract: - lang: eng text: The distance between Ca^2+ channels and release sensors determines the speed and efficacy of synaptic transmission. Tight "nanodomain" channel-sensor coupling initiates transmitter release at synapses in the mature brain, whereas loose "microdomain" coupling appears restricted to early developmental stages. To probe the coupling configuration at a plastic synapse in the mature central nervous system, we performed paired recordings between mossy fiber terminals and CA3 pyramidal neurons in rat hippocampus. Millimolar concentrations of both the fast Ca^2+ chelator BAPTA [1,2-bis(2-aminophenoxy)ethane- N,N, N′,N′-tetraacetic acid] and the slow chelator EGTA efficiently suppressed transmitter release, indicating loose coupling between Ca^2+ channels and release sensors. Loose coupling enabled the control of initial release probability by fast endogenous Ca^2+ buffers and the generation of facilitation by buffer saturation. Thus, loose coupling provides the molecular framework for presynaptic plasticity. author: - first_name: Nicholas full_name: Vyleta, Nicholas id: 36C4978E-F248-11E8-B48F-1D18A9856A87 last_name: Vyleta - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Vyleta N, Jonas PM. Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse. Science. 2014;343(6171):665-670. doi:10.1126/science.1244811 apa: Vyleta, N., & Jonas, P. M. (2014). Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.1244811 chicago: Vyleta, Nicholas, and Peter M Jonas. “Loose Coupling between Ca^2+ Channels and Release Sensors at a Plastic Hippocampal Synapse.” Science. American Association for the Advancement of Science, 2014. https://doi.org/10.1126/science.1244811. ieee: N. Vyleta and P. M. Jonas, “Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse,” Science, vol. 343, no. 6171. American Association for the Advancement of Science, pp. 665–670, 2014. ista: Vyleta N, Jonas PM. 2014. Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse. Science. 343(6171), 665–670. mla: Vyleta, Nicholas, and Peter M. Jonas. “Loose Coupling between Ca^2+ Channels and Release Sensors at a Plastic Hippocampal Synapse.” Science, vol. 343, no. 6171, American Association for the Advancement of Science, 2014, pp. 665–70, doi:10.1126/science.1244811. short: N. Vyleta, P.M. Jonas, Science 343 (2014) 665–670. date_created: 2018-12-11T11:56:27Z date_published: 2014-02-01T00:00:00Z date_updated: 2021-01-12T06:56:09Z day: '01' department: - _id: PeJo doi: 10.1126/science.1244811 ec_funded: 1 intvolume: ' 343' issue: '6171' language: - iso: eng main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617475/ month: '02' oa: 1 oa_version: Submitted Version page: 665 - 670 project: - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons publication: Science publication_identifier: issn: - '00368075' publication_status: published publisher: American Association for the Advancement of Science publist_id: '4732' quality_controlled: '1' scopus_import: 1 status: public title: Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 343 year: '2014' ... --- _id: '2254' abstract: - lang: eng text: Theta-gamma network oscillations are thought to represent key reference signals for information processing in neuronal ensembles, but the underlying synaptic mechanisms remain unclear. To address this question, we performed whole-cell (WC) patch-clamp recordings from mature hippocampal granule cells (GCs) in vivo in the dentate gyrus of anesthetized and awake rats. GCs in vivo fired action potentials at low frequency, consistent with sparse coding in the dentate gyrus. GCs were exposed to barrages of fast AMPAR-mediated excitatory postsynaptic currents (EPSCs), primarily relayed from the entorhinal cortex, and inhibitory postsynaptic currents (IPSCs), presumably generated by local interneurons. EPSCs exhibited coherence with the field potential predominantly in the theta frequency band, whereas IPSCs showed coherence primarily in the gamma range. Action potentials in GCs were phase locked to network oscillations. Thus, theta-gamma-modulated synaptic currents may provide a framework for sparse temporal coding of information in the dentate gyrus. author: - first_name: Alejandro full_name: Pernia-Andrade, Alejandro id: 36963E98-F248-11E8-B48F-1D18A9856A87 last_name: Pernia-Andrade - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Pernia-Andrade A, Jonas PM. Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations. Neuron. 2014;81(1):140-152. doi:10.1016/j.neuron.2013.09.046 apa: Pernia-Andrade, A., & Jonas, P. M. (2014). Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2013.09.046 chicago: Pernia-Andrade, Alejandro, and Peter M Jonas. “Theta-Gamma-Modulated Synaptic Currents in Hippocampal Granule Cells in Vivo Define a Mechanism for Network Oscillations.” Neuron. Elsevier, 2014. https://doi.org/10.1016/j.neuron.2013.09.046. ieee: A. Pernia-Andrade and P. M. Jonas, “Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations,” Neuron, vol. 81, no. 1. Elsevier, pp. 140–152, 2014. ista: Pernia-Andrade A, Jonas PM. 2014. Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations. Neuron. 81(1), 140–152. mla: Pernia-Andrade, Alejandro, and Peter M. Jonas. “Theta-Gamma-Modulated Synaptic Currents in Hippocampal Granule Cells in Vivo Define a Mechanism for Network Oscillations.” Neuron, vol. 81, no. 1, Elsevier, 2014, pp. 140–52, doi:10.1016/j.neuron.2013.09.046. short: A. Pernia-Andrade, P.M. Jonas, Neuron 81 (2014) 140–152. date_created: 2018-12-11T11:56:35Z date_published: 2014-01-08T00:00:00Z date_updated: 2021-01-12T06:56:19Z day: '08' ddc: - '570' department: - _id: PeJo doi: 10.1016/j.neuron.2013.09.046 ec_funded: 1 file: - access_level: open_access checksum: 438547cfcd9045a22f065f2019f07849 content_type: application/pdf creator: system date_created: 2018-12-12T10:09:48Z date_updated: 2020-07-14T12:45:35Z file_id: '4773' file_name: IST-2016-422-v1+1_1-s2.0-S0896627313009227-main.pdf file_size: 4373072 relation: main_file file_date_updated: 2020-07-14T12:45:35Z has_accepted_license: '1' intvolume: ' 81' issue: '1' language: - iso: eng month: '01' oa: 1 oa_version: Published Version page: 140 - 152 project: - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses publication: Neuron publication_identifier: issn: - '08966273' publication_status: published publisher: Elsevier publist_id: '4692' pubrep_id: '422' quality_controlled: '1' scopus_import: 1 status: public title: Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 81 year: '2014' ... --- _id: '2285' abstract: - lang: eng text: GABAergic inhibitory interneurons control fundamental aspects of neuronal network function. Their functional roles are assumed to be defined by the identity of their input synapses, the architecture of their dendritic tree, the passive and active membrane properties and finally the nature of their postsynaptic targets. Indeed, interneurons display a high degree of morphological and physiological heterogeneity. However, whether their morphological and physiological characteristics are correlated and whether interneuron diversity can be described by a continuum of GABAergic cell types or by distinct classes has remained unclear. Here we perform a detailed morphological and physiological characterization of GABAergic cells in the dentate gyrus, the input region of the hippocampus. To achieve an unbiased and efficient sampling and classification we used knock-in mice expressing the enhanced green fluorescent protein (eGFP) in glutamate decarboxylase 67 (GAD67)-positive neurons and performed cluster analysis. We identified five interneuron classes, each of them characterized by a distinct set of anatomical and physiological parameters. Cross-correlation analysis further revealed a direct relation between morphological and physiological properties indicating that dentate gyrus interneurons fall into functionally distinct classes which may differentially control neuronal network activity. acknowledgement: 'Funded by Deutsche Forschungsgemeinschaft. Grant Numbers: SFB 505, SFB 780, BA1582/2-1 Excellence Initiative of the German Research Foundation (Spemann Graduate School). Grant Number: GSC-4 Lichtenberg Professorship-Award (VW-Foundation); Schram-Foundation; Excellence Initiative Brain Links-Brain Tools. The authors thank Drs. Jonas-Frederic Sauer and Claudio Elgueta for critically reading the manuscript. They also thank Karin Winterhalter, Margit Northemann and Ulrich Nöller for technical assistance.' author: - first_name: Jonas full_name: Hosp, Jonas last_name: Hosp - first_name: Michael full_name: Strüber, Michael last_name: Strüber - first_name: Yuchio full_name: Yanagawa, Yuchio last_name: Yanagawa - first_name: Kunihiko full_name: Obata, Kunihiko last_name: Obata - first_name: Imre full_name: Vida, Imre last_name: Vida - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 - first_name: Marlene full_name: Bartos, Marlene last_name: Bartos citation: ama: Hosp J, Strüber M, Yanagawa Y, et al. Morpho-physiological criteria divide dentate gyrus interneurons into classes. Hippocampus. 2014;23(2):189-203. doi:10.1002/hipo.22214 apa: Hosp, J., Strüber, M., Yanagawa, Y., Obata, K., Vida, I., Jonas, P. M., & Bartos, M. (2014). Morpho-physiological criteria divide dentate gyrus interneurons into classes. Hippocampus. Wiley-Blackwell. https://doi.org/10.1002/hipo.22214 chicago: Hosp, Jonas, Michael Strüber, Yuchio Yanagawa, Kunihiko Obata, Imre Vida, Peter M Jonas, and Marlene Bartos. “Morpho-Physiological Criteria Divide Dentate Gyrus Interneurons into Classes.” Hippocampus. Wiley-Blackwell, 2014. https://doi.org/10.1002/hipo.22214. ieee: J. Hosp et al., “Morpho-physiological criteria divide dentate gyrus interneurons into classes,” Hippocampus, vol. 23, no. 2. Wiley-Blackwell, pp. 189–203, 2014. ista: Hosp J, Strüber M, Yanagawa Y, Obata K, Vida I, Jonas PM, Bartos M. 2014. Morpho-physiological criteria divide dentate gyrus interneurons into classes. Hippocampus. 23(2), 189–203. mla: Hosp, Jonas, et al. “Morpho-Physiological Criteria Divide Dentate Gyrus Interneurons into Classes.” Hippocampus, vol. 23, no. 2, Wiley-Blackwell, 2014, pp. 189–203, doi:10.1002/hipo.22214. short: J. Hosp, M. Strüber, Y. Yanagawa, K. Obata, I. Vida, P.M. Jonas, M. Bartos, Hippocampus 23 (2014) 189–203. date_created: 2018-12-11T11:56:46Z date_published: 2014-02-01T00:00:00Z date_updated: 2021-01-12T06:56:32Z day: '01' ddc: - '570' department: - _id: PeJo doi: 10.1002/hipo.22214 file: - access_level: open_access checksum: ff6bc75a79dbc985a2e31b79253e6444 content_type: application/pdf creator: system date_created: 2018-12-12T10:15:54Z date_updated: 2020-07-14T12:45:37Z file_id: '5178' file_name: IST-2016-461-v1+1_Hosp_et_al-2014-Hippocampus.pdf file_size: 801589 relation: main_file file_date_updated: 2020-07-14T12:45:37Z has_accepted_license: '1' intvolume: ' 23' issue: '2' language: - iso: eng month: '02' oa: 1 oa_version: Published Version page: 189 - 203 publication: Hippocampus publication_status: published publisher: Wiley-Blackwell publist_id: '4646' pubrep_id: '461' quality_controlled: '1' scopus_import: 1 status: public title: Morpho-physiological criteria divide dentate gyrus interneurons into classes tmp: image: /images/cc_by_nc.png legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) short: CC BY-NC (4.0) type: journal_article user_id: 3FFCCD3A-F248-11E8-B48F-1D18A9856A87 volume: 23 year: '2014' ... --- _id: '10396' abstract: - lang: eng text: Stimfit is a free cross-platform software package for viewing and analyzing electrophysiological data. It supports most standard file types for cellular neurophysiology and other biomedical formats. Its analysis algorithms have been used and validated in several experimental laboratories. Its embedded Python scripting interface makes Stimfit highly extensible and customizable. article_number: '000010151520134181' article_processing_charge: No article_type: original author: - first_name: Alois full_name: Schlögl, Alois id: 45BF87EE-F248-11E8-B48F-1D18A9856A87 last_name: Schlögl orcid: 0000-0002-5621-8100 - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 - first_name: C. full_name: Schmidt-Hieber, C. last_name: Schmidt-Hieber - first_name: S. J. full_name: Guzman, S. J. last_name: Guzman citation: ama: 'Schlögl A, Jonas PM, Schmidt-Hieber C, Guzman SJ. Stimfit: A fast visualization and analysis environment for cellular neurophysiology. Biomedical Engineering / Biomedizinische Technik. 2013;58(SI-1-Track-G). doi:10.1515/bmt-2013-4181' apa: 'Schlögl, A., Jonas, P. M., Schmidt-Hieber, C., & Guzman, S. J. (2013). Stimfit: A fast visualization and analysis environment for cellular neurophysiology. Biomedical Engineering / Biomedizinische Technik. Graz, Austria: De Gruyter. https://doi.org/10.1515/bmt-2013-4181' chicago: 'Schlögl, Alois, Peter M Jonas, C. Schmidt-Hieber, and S. J. Guzman. “Stimfit: A Fast Visualization and Analysis Environment for Cellular Neurophysiology.” Biomedical Engineering / Biomedizinische Technik. De Gruyter, 2013. https://doi.org/10.1515/bmt-2013-4181.' ieee: 'A. Schlögl, P. M. Jonas, C. Schmidt-Hieber, and S. J. Guzman, “Stimfit: A fast visualization and analysis environment for cellular neurophysiology,” Biomedical Engineering / Biomedizinische Technik, vol. 58, no. SI-1-Track-G. De Gruyter, 2013.' ista: 'Schlögl A, Jonas PM, Schmidt-Hieber C, Guzman SJ. 2013. Stimfit: A fast visualization and analysis environment for cellular neurophysiology. Biomedical Engineering / Biomedizinische Technik. 58(SI-1-Track-G), 000010151520134181.' mla: 'Schlögl, Alois, et al. “Stimfit: A Fast Visualization and Analysis Environment for Cellular Neurophysiology.” Biomedical Engineering / Biomedizinische Technik, vol. 58, no. SI-1-Track-G, 000010151520134181, De Gruyter, 2013, doi:10.1515/bmt-2013-4181.' short: A. Schlögl, P.M. Jonas, C. Schmidt-Hieber, S.J. Guzman, Biomedical Engineering / Biomedizinische Technik 58 (2013). conference: end_date: 2013-09-21 location: Graz, Austria name: 'BMT: Biomedizinische Technik ' start_date: 2013-09-19 date_created: 2021-12-01T14:35:35Z date_published: 2013-08-01T00:00:00Z date_updated: 2021-12-02T12:51:12Z day: '01' ddc: - '005' - '610' department: - _id: PeJo doi: 10.1515/bmt-2013-4181 external_id: pmid: - '24042795' file: - access_level: open_access checksum: cdfc5339b530a25d6079f7223f0b1f16 content_type: application/pdf creator: schloegl date_created: 2021-12-01T14:38:08Z date_updated: 2021-12-01T14:38:08Z file_id: '10397' file_name: Schloegl_Abstract-BMT2013.pdf file_size: 149825 relation: main_file success: 1 file_date_updated: 2021-12-01T14:38:08Z has_accepted_license: '1' intvolume: ' 58' issue: SI-1-Track-G keyword: - biomedical engineering - data analysis - free software language: - iso: eng month: '08' oa: 1 oa_version: Submitted Version pmid: 1 publication: Biomedical Engineering / Biomedizinische Technik publication_identifier: eissn: - 1862-278X issn: - 0013-5585 publication_status: published publisher: De Gruyter quality_controlled: '1' status: public title: 'Stimfit: A fast visualization and analysis environment for cellular neurophysiology' type: journal_article user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9 volume: 58 year: '2013' ... --- _id: '2954' abstract: - lang: eng text: Spontaneous postsynaptic currents (PSCs) provide key information about the mechanisms of synaptic transmission and the activity modes of neuronal networks. However, detecting spontaneous PSCs in vitro and in vivo has been challenging, because of the small amplitude, the variable kinetics, and the undefined time of generation of these events. Here, we describe a, to our knowledge, new method for detecting spontaneous synaptic events by deconvolution, using a template that approximates the average time course of spontaneous PSCs. A recorded PSC trace is deconvolved from the template, resulting in a series of delta-like functions. The maxima of these delta-like events are reliably detected, revealing the precise onset times of the spontaneous PSCs. Among all detection methods, the deconvolution-based method has a unique temporal resolution, allowing the detection of individual events in high-frequency bursts. Furthermore, the deconvolution-based method has a high amplitude resolution, because deconvolution can substantially increase the signal/noise ratio. When tested against previously published methods using experimental data, the deconvolution-based method was superior for spontaneous PSCs recorded in vivo. Using the high-resolution deconvolution-based detection algorithm, we show that the frequency of spontaneous excitatory postsynaptic currents in dentate gyrus granule cells is 4.5 times higher in vivo than in vitro. acknowledgement: "This work was supported by the Deutsche Forschungsgemeinschaft (TR3/B10) and a European Research Council Advanced grant to P.J.\r\nWe thank H. Hu, S. J. Guzman, and C. Schmidt-Hieber for critically reading the manuscript, I. Koeva and F. Marr for technical support, and E. Kramberger for editorial assistance.\r\n" author: - first_name: Alejandro full_name: Pernia-Andrade, Alejandro id: 36963E98-F248-11E8-B48F-1D18A9856A87 last_name: Pernia-Andrade - first_name: Sarit full_name: Goswami, Sarit id: 3A578F32-F248-11E8-B48F-1D18A9856A87 last_name: Goswami - first_name: Yvonne full_name: Stickler, Yvonne id: 63B76600-E9CC-11E9-9B5F-82450873F7A1 last_name: Stickler - first_name: Ulrich full_name: Fröbe, Ulrich last_name: Fröbe - first_name: Alois full_name: Schlögl, Alois id: 45BF87EE-F248-11E8-B48F-1D18A9856A87 last_name: Schlögl orcid: 0000-0002-5621-8100 - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Pernia-Andrade A, Goswami S, Stickler Y, Fröbe U, Schlögl A, Jonas PM. A deconvolution based method with high sensitivity and temporal resolution for detection of spontaneous synaptic currents in vitro and in vivo. Biophysical Journal. 2012;103(7):1429-1439. doi:10.1016/j.bpj.2012.08.039 apa: Pernia-Andrade, A., Goswami, S., Stickler, Y., Fröbe, U., Schlögl, A., & Jonas, P. M. (2012). A deconvolution based method with high sensitivity and temporal resolution for detection of spontaneous synaptic currents in vitro and in vivo. Biophysical Journal. Biophysical. https://doi.org/10.1016/j.bpj.2012.08.039 chicago: Pernia-Andrade, Alejandro, Sarit Goswami, Yvonne Stickler, Ulrich Fröbe, Alois Schlögl, and Peter M Jonas. “A Deconvolution Based Method with High Sensitivity and Temporal Resolution for Detection of Spontaneous Synaptic Currents in Vitro and in Vivo.” Biophysical Journal. Biophysical, 2012. https://doi.org/10.1016/j.bpj.2012.08.039. ieee: A. Pernia-Andrade, S. Goswami, Y. Stickler, U. Fröbe, A. Schlögl, and P. M. Jonas, “A deconvolution based method with high sensitivity and temporal resolution for detection of spontaneous synaptic currents in vitro and in vivo,” Biophysical Journal, vol. 103, no. 7. Biophysical, pp. 1429–1439, 2012. ista: Pernia-Andrade A, Goswami S, Stickler Y, Fröbe U, Schlögl A, Jonas PM. 2012. A deconvolution based method with high sensitivity and temporal resolution for detection of spontaneous synaptic currents in vitro and in vivo. Biophysical Journal. 103(7), 1429–1439. mla: Pernia-Andrade, Alejandro, et al. “A Deconvolution Based Method with High Sensitivity and Temporal Resolution for Detection of Spontaneous Synaptic Currents in Vitro and in Vivo.” Biophysical Journal, vol. 103, no. 7, Biophysical, 2012, pp. 1429–39, doi:10.1016/j.bpj.2012.08.039. short: A. Pernia-Andrade, S. Goswami, Y. Stickler, U. Fröbe, A. Schlögl, P.M. Jonas, Biophysical Journal 103 (2012) 1429–1439. date_created: 2018-12-11T12:00:32Z date_published: 2012-10-03T00:00:00Z date_updated: 2021-01-12T07:40:01Z day: '03' department: - _id: PeJo - _id: ScienComp doi: 10.1016/j.bpj.2012.08.039 external_id: pmid: - '23062335' intvolume: ' 103' issue: '7' language: - iso: eng main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3471482/ month: '10' oa: 1 oa_version: Submitted Version page: 1429 - 1439 pmid: 1 project: - _id: 25BDE9A4-B435-11E9-9278-68D0E5697425 grant_number: SFB-TR3-TP10B name: Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen publication: Biophysical Journal publication_status: published publisher: Biophysical publist_id: '3774' quality_controlled: '1' scopus_import: 1 status: public title: A deconvolution based method with high sensitivity and temporal resolution for detection of spontaneous synaptic currents in vitro and in vivo type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 103 year: '2012' ... --- _id: '2969' abstract: - lang: eng text: "The coupling between presynaptic Ca^(2+) channels and Ca^(2+) sensors of exocytosis is a key determinant of synaptic transmission. Evoked release from parvalbumin (PV)-expressing interneurons is triggered by nanodomain coupling of P/Q-type Ca^(2+) channels, whereas release from cholecystokinin (CCK)-containing interneurons is generated by microdomain coupling of N-type channels. Nanodomain coupling has several functional advantages, including speed and efficacy of transmission. One potential disadvantage is that stochastic\r\nopening of presynaptic Ca^(2+) channels may trigger spontaneous transmitter release. We addressed this possibility in rat hippocampal\r\ngranule cells, which receive converging inputs from different inhibitory sources. Both reduction of extracellular Ca^(2+) concentration and the unselective Ca^(2+) channel blocker Cd^(2+) reduced the frequency of miniature IPSCs (mIPSCs) in granule cells by ~50%, suggesting that the opening of presynaptic Ca^(2+) channels contributes to spontaneous release. Application of the selective P/Q-type Ca^(2+) channel blocker\r\nω-agatoxin IVa had no detectable effects, whereas both the N-type blocker ω-conotoxin GVIa and the L-type blocker nimodipine reduced\r\nmIPSC frequency. Furthermore, both the fast Ca^(2+) chelator BAPTA-AM and the slow chelator EGTA-AM reduced the mIPSC frequency,\r\nsuggesting that Ca^(2+)-dependent spontaneous release is triggered by microdomain rather than nanodomain coupling. The CB_(1) receptor\r\nagonist WIN 55212-2 also decreased spontaneous release; this effect was occluded by prior application of ω-conotoxin GVIa, suggesting that a major fraction of Ca^(2+)-dependent spontaneous release was generated at the terminals of CCK-expressing interneurons. Tonic inhibition generated by spontaneous opening of presynaptic N- and L-type Ca^(2+) channels may be important for hippocampal information processing.\r\n" acknowledgement: This work was supported by grants from the Deutsche Forschungsgemeinschaft (TR 3/B10, Leibniz program, GSC-4 Spemann Graduate School) and the European Union (European Research Council Advanced Grant). author: - first_name: Sarit full_name: Goswami, Sarit id: 3A578F32-F248-11E8-B48F-1D18A9856A87 last_name: Goswami - first_name: Iancu full_name: Bucurenciu, Iancu last_name: Bucurenciu - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Goswami S, Bucurenciu I, Jonas PM. Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling. Journal of Neuroscience. 2012;32(41):14294-14304. doi:10.1523/JNEUROSCI.6104-11.2012 apa: Goswami, S., Bucurenciu, I., & Jonas, P. M. (2012). Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.6104-11.2012 chicago: Goswami, Sarit, Iancu Bucurenciu, and Peter M Jonas. “Miniature IPSCs in Hippocampal Granule Cells Are Triggered by Voltage-Gated Ca^(2+) Channels via Microdomain Coupling.” Journal of Neuroscience. Society for Neuroscience, 2012. https://doi.org/10.1523/JNEUROSCI.6104-11.2012. ieee: S. Goswami, I. Bucurenciu, and P. M. Jonas, “Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling,” Journal of Neuroscience, vol. 32, no. 41. Society for Neuroscience, pp. 14294–14304, 2012. ista: Goswami S, Bucurenciu I, Jonas PM. 2012. Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling. Journal of Neuroscience. 32(41), 14294–14304. mla: Goswami, Sarit, et al. “Miniature IPSCs in Hippocampal Granule Cells Are Triggered by Voltage-Gated Ca^(2+) Channels via Microdomain Coupling.” Journal of Neuroscience, vol. 32, no. 41, Society for Neuroscience, 2012, pp. 14294–304, doi:10.1523/JNEUROSCI.6104-11.2012. short: S. Goswami, I. Bucurenciu, P.M. Jonas, Journal of Neuroscience 32 (2012) 14294–14304. date_created: 2018-12-11T12:00:36Z date_published: 2012-10-10T00:00:00Z date_updated: 2021-01-12T07:40:08Z day: '10' department: - _id: PeJo doi: 10.1523/JNEUROSCI.6104-11.2012 external_id: pmid: - '23055500' intvolume: ' 32' issue: '41' language: - iso: eng main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3632771/ month: '10' oa: 1 oa_version: Submitted Version page: 14294 - 14304 pmid: 1 project: - _id: 25BDE9A4-B435-11E9-9278-68D0E5697425 grant_number: SFB-TR3-TP10B name: Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen publication: Journal of Neuroscience publication_status: published publisher: Society for Neuroscience publist_id: '3744' quality_controlled: '1' scopus_import: 1 status: public title: Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 32 year: '2012' ... --- _id: '3121' abstract: - lang: eng text: Voltage-activated Ca(2+) channels (VACCs) mediate Ca(2+) influx to trigger action potential-evoked neurotransmitter release, but the mechanism by which Ca(2+) regulates spontaneous transmission is unclear. We found that VACCs are the major physiological triggers for spontaneous release at mouse neocortical inhibitory synapses. Moreover, despite the absence of a synchronizing action potential, we found that spontaneous fusion of a GABA-containing vesicle required the activation of multiple tightly coupled VACCs of variable type. acknowledgement: "The work was supported by the US National Institutes of Health (DA027110 and GM097433) and OCTRI. C.W. and N.P.V. were supported by a grant from the National Heart, Lung, and Blood Institute (T32HL033808).\r\nWe thank M. Andresen and K. Khodakhah for helpful comments. " author: - first_name: Courtney full_name: Williams, Courtney last_name: Williams - first_name: Wenyan full_name: Chen, Wenyan last_name: Chen - first_name: Chia full_name: Lee, Chia last_name: Lee - first_name: Daniel full_name: Yaeger, Daniel last_name: Yaeger - first_name: Nicholas full_name: Vyleta, Nicholas id: 36C4978E-F248-11E8-B48F-1D18A9856A87 last_name: Vyleta - first_name: Stephen full_name: Smith, Stephen last_name: Smith citation: ama: Williams C, Chen W, Lee C, Yaeger D, Vyleta N, Smith S. Coactivation of multiple tightly coupled calcium channels triggers spontaneous release of GABA. Nature Neuroscience. 2012;15(9):1195-1197. doi:10.1038/nn.3162 apa: Williams, C., Chen, W., Lee, C., Yaeger, D., Vyleta, N., & Smith, S. (2012). Coactivation of multiple tightly coupled calcium channels triggers spontaneous release of GABA. Nature Neuroscience. Nature Publishing Group. https://doi.org/10.1038/nn.3162 chicago: Williams, Courtney, Wenyan Chen, Chia Lee, Daniel Yaeger, Nicholas Vyleta, and Stephen Smith. “Coactivation of Multiple Tightly Coupled Calcium Channels Triggers Spontaneous Release of GABA.” Nature Neuroscience. Nature Publishing Group, 2012. https://doi.org/10.1038/nn.3162. ieee: C. Williams, W. Chen, C. Lee, D. Yaeger, N. Vyleta, and S. Smith, “Coactivation of multiple tightly coupled calcium channels triggers spontaneous release of GABA,” Nature Neuroscience, vol. 15, no. 9. Nature Publishing Group, pp. 1195–1197, 2012. ista: Williams C, Chen W, Lee C, Yaeger D, Vyleta N, Smith S. 2012. Coactivation of multiple tightly coupled calcium channels triggers spontaneous release of GABA. Nature Neuroscience. 15(9), 1195–1197. mla: Williams, Courtney, et al. “Coactivation of Multiple Tightly Coupled Calcium Channels Triggers Spontaneous Release of GABA.” Nature Neuroscience, vol. 15, no. 9, Nature Publishing Group, 2012, pp. 1195–97, doi:10.1038/nn.3162. short: C. Williams, W. Chen, C. Lee, D. Yaeger, N. Vyleta, S. Smith, Nature Neuroscience 15 (2012) 1195–1197. date_created: 2018-12-11T12:01:30Z date_published: 2012-09-01T00:00:00Z date_updated: 2021-01-12T07:41:12Z day: '01' department: - _id: PeJo doi: 10.1038/nn.3162 external_id: pmid: - '22842148' intvolume: ' 15' issue: '9' language: - iso: eng main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3431448/ month: '09' oa: 1 oa_version: Submitted Version page: 1195 - 1197 pmid: 1 publication: Nature Neuroscience publication_status: published publisher: Nature Publishing Group publist_id: '3578' quality_controlled: '1' scopus_import: 1 status: public title: Coactivation of multiple tightly coupled calcium channels triggers spontaneous release of GABA type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 15 year: '2012' ... --- _id: '3317' abstract: - lang: eng text: The physical distance between presynaptic Ca2+ channels and the Ca2+ sensors that trigger exocytosis of neurotransmitter-containing vesicles is a key determinant of the signalling properties of synapses in the nervous system. Recent functional analysis indicates that in some fast central synapses, transmitter release is triggered by a small number of Ca2+ channels that are coupled to Ca2+ sensors at the nanometre scale. Molecular analysis suggests that this tight coupling is generated by protein–protein interactions involving Ca2+ channels, Ca2+ sensors and various other synaptic proteins. Nanodomain coupling has several functional advantages, as it increases the efficacy, speed and energy efficiency of synaptic transmission. acknowledgement: "Work of the authors was funded by grants of the Deutsche Forschungsgemeinschaft to P.J. (grants SFB 780/A5, TR 3/B10 and the Leibniz programme), a European Research Council Advanced grant to P.J. and a Swiss National Foundation fellowship to E.E.\r\nWe thank D. Tsien and E. Neher for their comments on this Review, J. Guzmán and A. Pernía-Andrade for reading earlier versions and E. Kramberger for perfect editorial support. We apologize that owing to space constraints, not all relevant papers could be cited.\r\n" author: - first_name: Emmanuel full_name: Eggermann, Emmanuel id: 34DACA34-E9AE-11E9-849C-D35BD8ADC20C last_name: Eggermann - first_name: Iancu full_name: Bucurenciu, Iancu id: 4BD1D872-E9AE-11E9-9EE9-8BF4597A9E2A last_name: Bucurenciu - first_name: Sarit full_name: Goswami, Sarit id: 3A578F32-F248-11E8-B48F-1D18A9856A87 last_name: Goswami - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Eggermann E, Bucurenciu I, Goswami S, Jonas PM. Nanodomain coupling between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses. Nature Reviews Neuroscience. 2012;13(1):7-21. doi:10.1038/nrn3125 apa: Eggermann, E., Bucurenciu, I., Goswami, S., & Jonas, P. M. (2012). Nanodomain coupling between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses. Nature Reviews Neuroscience. Nature Publishing Group. https://doi.org/10.1038/nrn3125 chicago: Eggermann, Emmanuel, Iancu Bucurenciu, Sarit Goswami, and Peter M Jonas. “Nanodomain Coupling between Ca(2+) Channels and Sensors of Exocytosis at Fast Mammalian Synapses.” Nature Reviews Neuroscience. Nature Publishing Group, 2012. https://doi.org/10.1038/nrn3125. ieee: E. Eggermann, I. Bucurenciu, S. Goswami, and P. M. Jonas, “Nanodomain coupling between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses,” Nature Reviews Neuroscience, vol. 13, no. 1. Nature Publishing Group, pp. 7–21, 2012. ista: Eggermann E, Bucurenciu I, Goswami S, Jonas PM. 2012. Nanodomain coupling between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses. Nature Reviews Neuroscience. 13(1), 7–21. mla: Eggermann, Emmanuel, et al. “Nanodomain Coupling between Ca(2+) Channels and Sensors of Exocytosis at Fast Mammalian Synapses.” Nature Reviews Neuroscience, vol. 13, no. 1, Nature Publishing Group, 2012, pp. 7–21, doi:10.1038/nrn3125. short: E. Eggermann, I. Bucurenciu, S. Goswami, P.M. Jonas, Nature Reviews Neuroscience 13 (2012) 7–21. date_created: 2018-12-11T12:02:38Z date_published: 2012-01-01T00:00:00Z date_updated: 2021-01-12T07:42:36Z day: '01' ddc: - '570' department: - _id: PeJo doi: 10.1038/nrn3125 file: - access_level: open_access checksum: 4c1c86b2f6e4e1562f5bb800b457ea9f content_type: application/pdf creator: system date_created: 2018-12-12T10:12:13Z date_updated: 2020-07-14T12:46:07Z file_id: '4931' file_name: IST-2017-820-v1+1_17463_3_art_file_109404_ltmxbw.pdf file_size: 314246 relation: main_file - access_level: open_access checksum: bceb2efdd49d115f4dde8486bc1be3f2 content_type: application/pdf creator: system date_created: 2018-12-12T10:12:14Z date_updated: 2020-07-14T12:46:07Z file_id: '4932' file_name: IST-2017-820-v1+2_17463_3_figure_109402_ltmwlp.pdf file_size: 1840216 relation: main_file file_date_updated: 2020-07-14T12:46:07Z has_accepted_license: '1' intvolume: ' 13' issue: '1' language: - iso: eng month: '01' oa: 1 oa_version: Submitted Version page: 7 - 21 project: - _id: 25BC64A8-B435-11E9-9278-68D0E5697425 grant_number: JO_780/A5 name: Synaptic Mechanisms of Neuronal Network Function - _id: 25BDE9A4-B435-11E9-9278-68D0E5697425 grant_number: SFB-TR3-TP10B name: Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen publication: Nature Reviews Neuroscience publication_status: published publisher: Nature Publishing Group publist_id: '3322' pubrep_id: '820' quality_controlled: '1' scopus_import: 1 status: public title: Nanodomain coupling between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 13 year: '2012' ... --- _id: '493' abstract: - lang: eng text: 'The BCI competition IV stands in the tradition of prior BCI competitions that aim to provide high quality neuroscientific data for open access to the scientific community. As experienced already in prior competitions not only scientists from the narrow field of BCI compete, but scholars with a broad variety of backgrounds and nationalities. They include high specialists as well as students.The goals of all BCI competitions have always been to challenge with respect to novel paradigms and complex data. We report on the following challenges: (1) asynchronous data, (2) synthetic, (3) multi-class continuous data, (4) sessionto-session transfer, (5) directionally modulated MEG, (6) finger movements recorded by ECoG. As after past competitions, our hope is that winning entries may enhance the analysis methods of future BCIs.' acknowledgement: "The studies were in part or completely supported by the Bundesministerium für Bildung und Forschung (BMBF), Fkz 01IB001A, 01GQ0850, by the German Science Foundation (DFG, contract MU 987/3-2), by the European ICT Programme Projects FP7-224631 and 216886, the World Class University Program through the National Research Foundation of Korea funded by the Ministry of Education, Science, and Technology (Grant R31-10008), the US Army Research Office [W911NF-08-1-0216 (Gerwin Schalk) and W911NF-07-1-0415 (Gerwin Schalk)] and the NIH [EB006356 (Gerwin Schalk) and EB000856 (Gerwin Schalk), the WIN-Kolleg of the Heidelberg Academy of Sciences and Humanities, German Federal Ministry of Education and Research grants 01GQ0420, 01GQ0761, 01GQ0762, and 01GQ0830, German Research Foundation grants 550/B5 and C6, and by a scholarship from the German National Academic Foundation. This paper only reflects the authors’ views and funding agencies are not liable for any use that may be made of the information contained herein.\r\n" article_number: '55' author: - first_name: Michael full_name: Tangermann, Michael last_name: Tangermann - first_name: Klaus full_name: Müller, Klaus last_name: Müller - first_name: Ad full_name: Aertsen, Ad last_name: Aertsen - first_name: Niels full_name: Birbaumer, Niels last_name: Birbaumer - first_name: Christoph full_name: Braun, Christoph last_name: Braun - first_name: Clemens full_name: Brunner, Clemens last_name: Brunner - first_name: Robert full_name: Leeb, Robert last_name: Leeb - first_name: Carsten full_name: Mehring, Carsten last_name: Mehring - first_name: Kai full_name: Miller, Kai last_name: Miller - first_name: Gernot full_name: Müller Putz, Gernot last_name: Müller Putz - first_name: Guido full_name: Nolte, Guido last_name: Nolte - first_name: Gert full_name: Pfurtscheller, Gert last_name: Pfurtscheller - first_name: Hubert full_name: Preissl, Hubert last_name: Preissl - first_name: Gerwin full_name: Schalk, Gerwin last_name: Schalk - first_name: Alois full_name: Schlögl, Alois id: 45BF87EE-F248-11E8-B48F-1D18A9856A87 last_name: Schlögl orcid: 0000-0002-5621-8100 - first_name: Carmen full_name: Vidaurre, Carmen last_name: Vidaurre - first_name: Stephan full_name: Waldert, Stephan last_name: Waldert - first_name: Benjamin full_name: Blankertz, Benjamin last_name: Blankertz citation: ama: Tangermann M, Müller K, Aertsen A, et al. Review of the BCI competition IV. Frontiers in Neuroscience. 2012;6. doi:10.3389/fnins.2012.00055 apa: Tangermann, M., Müller, K., Aertsen, A., Birbaumer, N., Braun, C., Brunner, C., … Blankertz, B. (2012). Review of the BCI competition IV. Frontiers in Neuroscience. Frontiers Research Foundation. https://doi.org/10.3389/fnins.2012.00055 chicago: Tangermann, Michael, Klaus Müller, Ad Aertsen, Niels Birbaumer, Christoph Braun, Clemens Brunner, Robert Leeb, et al. “Review of the BCI Competition IV.” Frontiers in Neuroscience. Frontiers Research Foundation, 2012. https://doi.org/10.3389/fnins.2012.00055. ieee: M. Tangermann et al., “Review of the BCI competition IV,” Frontiers in Neuroscience, vol. 6. Frontiers Research Foundation, 2012. ista: Tangermann M, Müller K, Aertsen A, Birbaumer N, Braun C, Brunner C, Leeb R, Mehring C, Miller K, Müller Putz G, Nolte G, Pfurtscheller G, Preissl H, Schalk G, Schlögl A, Vidaurre C, Waldert S, Blankertz B. 2012. Review of the BCI competition IV. Frontiers in Neuroscience. 6, 55. mla: Tangermann, Michael, et al. “Review of the BCI Competition IV.” Frontiers in Neuroscience, vol. 6, 55, Frontiers Research Foundation, 2012, doi:10.3389/fnins.2012.00055. short: M. Tangermann, K. Müller, A. Aertsen, N. Birbaumer, C. Braun, C. Brunner, R. Leeb, C. Mehring, K. Miller, G. Müller Putz, G. Nolte, G. Pfurtscheller, H. Preissl, G. Schalk, A. Schlögl, C. Vidaurre, S. Waldert, B. Blankertz, Frontiers in Neuroscience 6 (2012). date_created: 2018-12-11T11:46:46Z date_published: 2012-07-13T00:00:00Z date_updated: 2021-01-12T08:01:03Z day: '13' ddc: - '004' department: - _id: ScienComp - _id: PeJo doi: 10.3389/fnins.2012.00055 file: - access_level: open_access checksum: 195238221c4b0b0f4035f6f6c16ea17c content_type: application/pdf creator: system date_created: 2018-12-12T10:18:34Z date_updated: 2020-07-14T12:46:35Z file_id: '5356' file_name: IST-2018-945-v1+1_2012_Schloegl_Review_of.pdf file_size: 2693701 relation: main_file file_date_updated: 2020-07-14T12:46:35Z has_accepted_license: '1' intvolume: ' 6' language: - iso: eng month: '07' oa: 1 oa_version: Published Version publication: Frontiers in Neuroscience publication_status: published publisher: Frontiers Research Foundation publist_id: '7327' pubrep_id: '945' quality_controlled: '1' scopus_import: 1 status: public title: Review of the BCI competition IV tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 6 year: '2012' ... --- _id: '3258' abstract: - lang: eng text: CA3 pyramidal neurons are important for memory formation and pattern completion in the hippocampal network. It is generally thought that proximal synapses from the mossy fibers activate these neurons most efficiently, whereas distal inputs from the perforant path have a weaker modulatory influence. We used confocally targeted patch-clamp recording from dendrites and axons to map the activation of rat CA3 pyramidal neurons at the subcellular level. Our results reveal two distinct dendritic domains. In the proximal domain, action potentials initiated in the axon backpropagate actively with large amplitude and fast time course. In the distal domain, Na+ channel–mediated dendritic spikes are efficiently initiated by waveforms mimicking synaptic events. CA3 pyramidal neuron dendrites showed a high Na+-to-K+ conductance density ratio, providing ideal conditions for active backpropagation and dendritic spike initiation. Dendritic spikes may enhance the computational power of CA3 pyramidal neurons in the hippocampal network. acknowledgement: This work was supported by the Deutsche Forschungsgemeinschaft (TR 3/B10) and the European Union (European Research Council Advanced grant to P.J.). article_processing_charge: No article_type: original author: - first_name: Sooyun full_name: Kim, Sooyun id: 394AB1C8-F248-11E8-B48F-1D18A9856A87 last_name: Kim - first_name: José full_name: Guzmán, José id: 30CC5506-F248-11E8-B48F-1D18A9856A87 last_name: Guzmán orcid: 0000-0003-2209-5242 - first_name: Hua full_name: Hu, Hua id: 4AC0145C-F248-11E8-B48F-1D18A9856A87 last_name: Hu - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Kim S, Guzmán J, Hu H, Jonas PM. Active dendrites support efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons. Nature Neuroscience. 2012;15(4):600-606. doi:10.1038/nn.3060 apa: Kim, S., Guzmán, J., Hu, H., & Jonas, P. M. (2012). Active dendrites support efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons. Nature Neuroscience. Nature Publishing Group. https://doi.org/10.1038/nn.3060 chicago: Kim, Sooyun, José Guzmán, Hua Hu, and Peter M Jonas. “Active Dendrites Support Efficient Initiation of Dendritic Spikes in Hippocampal CA3 Pyramidal Neurons.” Nature Neuroscience. Nature Publishing Group, 2012. https://doi.org/10.1038/nn.3060. ieee: S. Kim, J. Guzmán, H. Hu, and P. M. Jonas, “Active dendrites support efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons,” Nature Neuroscience, vol. 15, no. 4. Nature Publishing Group, pp. 600–606, 2012. ista: Kim S, Guzmán J, Hu H, Jonas PM. 2012. Active dendrites support efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons. Nature Neuroscience. 15(4), 600–606. mla: Kim, Sooyun, et al. “Active Dendrites Support Efficient Initiation of Dendritic Spikes in Hippocampal CA3 Pyramidal Neurons.” Nature Neuroscience, vol. 15, no. 4, Nature Publishing Group, 2012, pp. 600–06, doi:10.1038/nn.3060. short: S. Kim, J. Guzmán, H. Hu, P.M. Jonas, Nature Neuroscience 15 (2012) 600–606. date_created: 2018-12-11T12:02:18Z date_published: 2012-04-01T00:00:00Z date_updated: 2023-09-07T11:43:52Z day: '01' department: - _id: PeJo doi: 10.1038/nn.3060 external_id: pmid: - '22388958' intvolume: ' 15' issue: '4' language: - iso: eng main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617474/ month: '04' oa: 1 oa_version: Published Version page: 600 - 606 pmid: 1 project: - _id: 25BDE9A4-B435-11E9-9278-68D0E5697425 grant_number: SFB-TR3-TP10B name: Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen publication: Nature Neuroscience publication_identifier: issn: - 1546-1726 publication_status: published publisher: Nature Publishing Group publist_id: '3390' quality_controlled: '1' related_material: record: - id: '2964' relation: dissertation_contains status: public scopus_import: '1' status: public title: Active dendrites support efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons type: journal_article user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9 volume: 15 year: '2012' ... --- _id: '2964' abstract: - lang: eng text: 'CA3 pyramidal neurons are important for memory formation and pattern completion in the hippocampal network. These neurons receive multiple excitatory inputs from numerous sources. Therefore, the rules of spatiotemporal integration of multiple synaptic inputs and propagation of action potentials are important to understand how CA3 neurons contribute to higher brain functions at cellular level. By using confocally targeted patch-clamp recording techniques, we investigated the biophysical properties of rat CA3 pyramidal neuron dendrites. We found two distinct dendritic domains critical for action potential initiation and propagation: In the proximal domain, action potentials initiated in the axon backpropagate actively with large amplitude and fast time course. In the distal domain, Na+-channel mediated dendritic spikes are efficiently evoked by local dendritic depolarization or waveforms mimicking synaptic events. These findings can be explained by a high Na+-to-K+ conductance density ratio of CA3 pyramidal neuron dendrites. The results challenge the prevailing view that proximal mossy fiber inputs activate CA3 pyramidal neurons more efficiently than distal perforant inputs by showing that the distal synapses trigger a different form of activity represented by dendritic spikes. The high probability of dendritic spike initiation in the distal area may enhance the computational power of CA3 pyramidal neurons in the hippocampal network. ' alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Sooyun full_name: Kim, Sooyun id: 394AB1C8-F248-11E8-B48F-1D18A9856A87 last_name: Kim citation: ama: Kim S. Active properties of hippocampal CA3 pyramidal neuron dendrites. 2012. apa: Kim, S. (2012). Active properties of hippocampal CA3 pyramidal neuron dendrites. Institute of Science and Technology Austria. chicago: Kim, Sooyun. “Active Properties of Hippocampal CA3 Pyramidal Neuron Dendrites.” Institute of Science and Technology Austria, 2012. ieee: S. Kim, “Active properties of hippocampal CA3 pyramidal neuron dendrites,” Institute of Science and Technology Austria, 2012. ista: Kim S. 2012. Active properties of hippocampal CA3 pyramidal neuron dendrites. Institute of Science and Technology Austria. mla: Kim, Sooyun. Active Properties of Hippocampal CA3 Pyramidal Neuron Dendrites. Institute of Science and Technology Austria, 2012. short: S. Kim, Active Properties of Hippocampal CA3 Pyramidal Neuron Dendrites, Institute of Science and Technology Austria, 2012. date_created: 2018-12-11T12:00:35Z date_published: 2012-06-01T00:00:00Z date_updated: 2023-09-07T11:43:51Z day: '01' degree_awarded: PhD department: - _id: PeJo - _id: GradSch language: - iso: eng month: '06' oa_version: None page: '65' publication_identifier: issn: - 2663-337X publication_status: published publisher: Institute of Science and Technology Austria publist_id: '3755' related_material: record: - id: '3258' relation: part_of_dissertation status: public status: public supervisor: - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 title: Active properties of hippocampal CA3 pyramidal neuron dendrites type: dissertation user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9 year: '2012' ... --- _id: '3318' abstract: - lang: eng text: Parvalbumin is thought to act in a manner similar to EGTA, but how a slow Ca2+ buffer affects nanodomain-coupling regimes at GABAergic synapses is unclear. Direct measurements of parvalbumin concentration and paired recordings in rodent hippocampus and cerebellum revealed that parvalbumin affects synaptic dynamics only when expressed at high levels. Modeling suggests that, in high concentrations, parvalbumin may exert BAPTA-like effects, modulating nanodomain coupling via competition with local saturation of endogenous fixed buffers. author: - first_name: Emmanuel full_name: Eggermann, Emmanuel last_name: Eggermann - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Eggermann E, Jonas PM. How the “slow” Ca(2+) buffer parvalbumin affects transmitter release in nanodomain coupling regimes at GABAergic synapses. Nature Neuroscience. 2011;15:20-22. doi:10.1038/nn.3002 apa: Eggermann, E., & Jonas, P. M. (2011). How the “slow” Ca(2+) buffer parvalbumin affects transmitter release in nanodomain coupling regimes at GABAergic synapses. Nature Neuroscience. Nature Publishing Group. https://doi.org/10.1038/nn.3002 chicago: Eggermann, Emmanuel, and Peter M Jonas. “How the ‘Slow’ Ca(2+) Buffer Parvalbumin Affects Transmitter Release in Nanodomain Coupling Regimes at GABAergic Synapses.” Nature Neuroscience. Nature Publishing Group, 2011. https://doi.org/10.1038/nn.3002. ieee: E. Eggermann and P. M. Jonas, “How the ‘slow’ Ca(2+) buffer parvalbumin affects transmitter release in nanodomain coupling regimes at GABAergic synapses,” Nature Neuroscience, vol. 15. Nature Publishing Group, pp. 20–22, 2011. ista: Eggermann E, Jonas PM. 2011. How the “slow” Ca(2+) buffer parvalbumin affects transmitter release in nanodomain coupling regimes at GABAergic synapses. Nature Neuroscience. 15, 20–22. mla: Eggermann, Emmanuel, and Peter M. Jonas. “How the ‘Slow’ Ca(2+) Buffer Parvalbumin Affects Transmitter Release in Nanodomain Coupling Regimes at GABAergic Synapses.” Nature Neuroscience, vol. 15, Nature Publishing Group, 2011, pp. 20–22, doi:10.1038/nn.3002. short: E. Eggermann, P.M. Jonas, Nature Neuroscience 15 (2011) 20–22. date_created: 2018-12-11T12:02:38Z date_published: 2011-12-04T00:00:00Z date_updated: 2021-01-12T07:42:37Z day: '04' department: - _id: PeJo doi: 10.1038/nn.3002 intvolume: ' 15' language: - iso: eng main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3631701/ month: '12' oa: 1 oa_version: Submitted Version page: 20 - 22 publication: Nature Neuroscience publication_status: published publisher: Nature Publishing Group publist_id: '3321' quality_controlled: '1' scopus_import: 1 status: public title: How the “slow” Ca(2+) buffer parvalbumin affects transmitter release in nanodomain coupling regimes at GABAergic synapses type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 15 year: '2011' ... --- _id: '3369' abstract: - lang: eng text: Rab3 interacting molecules (RIMs) are highly enriched in the active zones of presynaptic terminals. It is generally thought that they operate as effectors of the small G protein Rab3. Three recent papers, by Han et al. (this issue of Neuron), Deng et al. (this issue of Neuron), and Kaeser et al. (a recent issue of Cell), shed new light on the functional role of RIM in presynaptic terminals. First, RIM tethers Ca2+ channels to active zones. Second, RIM contributes to priming of synaptic vesicles by interacting with another presynaptic protein, Munc13. author: - first_name: Alejandro full_name: Pernia-Andrade, Alejandro id: 36963E98-F248-11E8-B48F-1D18A9856A87 last_name: Pernia-Andrade - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Pernia-Andrade A, Jonas PM. The multiple faces of RIM. Neuron. 2011;69(2):185-187. doi:10.1016/j.neuron.2011.01.010 apa: Pernia-Andrade, A., & Jonas, P. M. (2011). The multiple faces of RIM. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2011.01.010 chicago: Pernia-Andrade, Alejandro, and Peter M Jonas. “The Multiple Faces of RIM.” Neuron. Elsevier, 2011. https://doi.org/10.1016/j.neuron.2011.01.010. ieee: A. Pernia-Andrade and P. M. Jonas, “The multiple faces of RIM,” Neuron, vol. 69, no. 2. Elsevier, pp. 185–187, 2011. ista: Pernia-Andrade A, Jonas PM. 2011. The multiple faces of RIM. Neuron. 69(2), 185–187. mla: Pernia-Andrade, Alejandro, and Peter M. Jonas. “The Multiple Faces of RIM.” Neuron, vol. 69, no. 2, Elsevier, 2011, pp. 185–87, doi:10.1016/j.neuron.2011.01.010. short: A. Pernia-Andrade, P.M. Jonas, Neuron 69 (2011) 185–187. date_created: 2018-12-11T12:02:56Z date_published: 2011-01-27T00:00:00Z date_updated: 2021-01-12T07:43:00Z day: '27' department: - _id: PeJo doi: 10.1016/j.neuron.2011.01.010 intvolume: ' 69' issue: '2' language: - iso: eng month: '01' oa_version: None page: 185 - 187 publication: Neuron publication_status: published publisher: Elsevier publist_id: '3243' quality_controlled: '1' scopus_import: 1 status: public title: The multiple faces of RIM type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 69 year: '2011' ... --- _id: '469' abstract: - lang: eng text: 'Spontaneous release of glutamate is important for maintaining synaptic strength and controlling spike timing in the brain. Mechanisms regulating spontaneous exocytosis remain poorly understood. Extracellular calcium concentration ([Ca2+]o) regulates Ca2+ entry through voltage-activated calcium channels (VACCs) and consequently is a pivotal determinant of action potential-evoked vesicle fusion. Extracellular Ca 2+ also enhances spontaneous release, but via unknown mechanisms. Here we report that external Ca2+ triggers spontaneous glutamate release more weakly than evoked release in mouse neocortical neurons. Blockade of VACCs has no effect on the spontaneous release rate or its dependence on [Ca2+]o. Intracellular [Ca2+] slowly increases in a minority of neurons following increases in [Ca2+]o. Furthermore, the enhancement of spontaneous release by extracellular calcium is insensitive to chelation of intracellular calcium by BAPTA. Activation of the calcium-sensing receptor (CaSR), a G-protein-coupled receptor present in nerve terminals, by several specific agonists increased spontaneous glutamate release. The frequency of spontaneous synaptic transmission was decreased in CaSR mutant neurons. The concentration-effect relationship for extracellular calcium regulation of spontaneous release was well described by a combination of CaSR-dependent and CaSR-independent mechanisms. Overall these results indicate that extracellular Ca2+ does not trigger spontaneous glutamate release by simply increasing calcium influx but stimulates CaSR and thereby promotes resting spontaneous glutamate release. ' author: - first_name: Nicholas full_name: Vyleta, Nicholas id: 36C4978E-F248-11E8-B48F-1D18A9856A87 last_name: Vyleta - first_name: Stephen full_name: Smith, Stephen last_name: Smith citation: ama: Vyleta N, Smith S. Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor. European Journal of Neuroscience. 2011;31(12):4593-4606. doi:10.1523/JNEUROSCI.6398-10.2011 apa: Vyleta, N., & Smith, S. (2011). Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor. European Journal of Neuroscience. Wiley-Blackwell. https://doi.org/10.1523/JNEUROSCI.6398-10.2011 chicago: Vyleta, Nicholas, and Stephen Smith. “Spontaneous Glutamate Release Is Independent of Calcium Influx and Tonically Activated by the Calcium-Sensing Receptor.” European Journal of Neuroscience. Wiley-Blackwell, 2011. https://doi.org/10.1523/JNEUROSCI.6398-10.2011. ieee: N. Vyleta and S. Smith, “Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor,” European Journal of Neuroscience, vol. 31, no. 12. Wiley-Blackwell, pp. 4593–4606, 2011. ista: Vyleta N, Smith S. 2011. Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor. European Journal of Neuroscience. 31(12), 4593–4606. mla: Vyleta, Nicholas, and Stephen Smith. “Spontaneous Glutamate Release Is Independent of Calcium Influx and Tonically Activated by the Calcium-Sensing Receptor.” European Journal of Neuroscience, vol. 31, no. 12, Wiley-Blackwell, 2011, pp. 4593–606, doi:10.1523/JNEUROSCI.6398-10.2011. short: N. Vyleta, S. Smith, European Journal of Neuroscience 31 (2011) 4593–4606. date_created: 2018-12-11T11:46:39Z date_published: 2011-03-23T00:00:00Z date_updated: 2021-01-12T08:00:49Z day: '23' department: - _id: PeJo doi: 10.1523/JNEUROSCI.6398-10.2011 intvolume: ' 31' issue: '12' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3097128/ month: '03' oa: 1 oa_version: Submitted Version page: 4593 - 4606 publication: European Journal of Neuroscience publication_status: published publisher: Wiley-Blackwell publist_id: '7353' quality_controlled: '1' scopus_import: 1 status: public title: Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 31 year: '2011' ... --- _id: '490' abstract: - lang: eng text: 'BioSig is an open source software library for biomedical signal processing. The aim of the BioSig project is to foster research in biomedical signal processing by providing free and open source software tools for many different application areas. Some of the areas where BioSig can be employed are neuroinformatics, brain-computer interfaces, neurophysiology, psychology, cardiovascular systems, and sleep research. Moreover, the analysis of biosignals such as the electroencephalogram (EEG), electrocorticogram (ECoG), electrocardiogram (ECG), electrooculogram (EOG), electromyogram (EMG), or respiration signals is a very relevant element of the BioSig project. Specifically, BioSig provides solutions for data acquisition, artifact processing, quality control, feature extraction, classification, modeling, and data visualization, to name a few. In this paper, we highlight several methods to help students and researchers to work more efficiently with biomedical signals. ' article_number: '935364' author: - first_name: Alois full_name: Schlögl, Alois id: 45BF87EE-F248-11E8-B48F-1D18A9856A87 last_name: Schlögl orcid: 0000-0002-5621-8100 - first_name: Carmen full_name: Vidaurre, Carmen last_name: Vidaurre - first_name: Tilmann full_name: Sander, Tilmann last_name: Sander citation: ama: 'Schlögl A, Vidaurre C, Sander T. BioSig: The free and open source software library for biomedical signal processing. Computational Intelligence and Neuroscience. 2011;2011. doi:10.1155/2011/935364' apa: 'Schlögl, A., Vidaurre, C., & Sander, T. (2011). BioSig: The free and open source software library for biomedical signal processing. Computational Intelligence and Neuroscience. Hindawi Publishing Corporation. https://doi.org/10.1155/2011/935364' chicago: 'Schlögl, Alois, Carmen Vidaurre, and Tilmann Sander. “BioSig: The Free and Open Source Software Library for Biomedical Signal Processing.” Computational Intelligence and Neuroscience. Hindawi Publishing Corporation, 2011. https://doi.org/10.1155/2011/935364.' ieee: 'A. Schlögl, C. Vidaurre, and T. Sander, “BioSig: The free and open source software library for biomedical signal processing,” Computational Intelligence and Neuroscience, vol. 2011. Hindawi Publishing Corporation, 2011.' ista: 'Schlögl A, Vidaurre C, Sander T. 2011. BioSig: The free and open source software library for biomedical signal processing. Computational Intelligence and Neuroscience. 2011, 935364.' mla: 'Schlögl, Alois, et al. “BioSig: The Free and Open Source Software Library for Biomedical Signal Processing.” Computational Intelligence and Neuroscience, vol. 2011, 935364, Hindawi Publishing Corporation, 2011, doi:10.1155/2011/935364.' short: A. Schlögl, C. Vidaurre, T. Sander, Computational Intelligence and Neuroscience 2011 (2011). date_created: 2018-12-11T11:46:45Z date_published: 2011-01-01T00:00:00Z date_updated: 2021-01-12T08:01:02Z day: '01' ddc: - '005' department: - _id: ScienComp - _id: PeJo doi: 10.1155/2011/935364 file: - access_level: open_access checksum: 8263bbf255171f2054f43f3db5f53b6e content_type: application/pdf creator: system date_created: 2018-12-12T10:07:44Z date_updated: 2020-07-14T12:46:35Z file_id: '4642' file_name: IST-2018-947-v1+1_2011_Schloegl_BioSig.pdf file_size: 2863551 relation: main_file file_date_updated: 2020-07-14T12:46:35Z has_accepted_license: '1' intvolume: ' 2011' language: - iso: eng month: '01' oa: 1 oa_version: Published Version publication: Computational Intelligence and Neuroscience publication_status: published publisher: Hindawi Publishing Corporation publist_id: '7330' pubrep_id: '947' quality_controlled: '1' scopus_import: 1 status: public title: 'BioSig: The free and open source software library for biomedical signal processing' tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 2011 year: '2011' ... --- _id: '3718' abstract: - lang: eng text: Long-term depression (LTD) is a form of synaptic plasticity that may contribute to information storage in the central nervous system. Here we report that LTD can be elicited in layer 5 pyramidal neurons of the rat prefrontal cortex by pairing low frequency stimulation with a modest postsynaptic depolarization. The induction of LTD required the activation of both metabotropic glutamate receptors of the mGlu1 subtype and voltage-sensitive Ca(2+) channels (VSCCs) of the T/R, P/Q and N types, leading to the stimulation of intracellular inositol trisphosphate (IP3) receptors by IP3 and Ca(2+). The subsequent release of Ca(2+) from intracellular stores activated the protein phosphatase cascade involving calcineurin and protein phosphatase 1. The activation of purinergic P2Y(1) receptors blocked LTD. This effect was prevented by P2Y(1) receptor antagonists and was absent in mice lacking P2Y(1) but not P2Y(2) receptors. We also found that activation of P2Y(1) receptors inhibits Ca(2+) transients via VSCCs in the apical dendrites and spines of pyramidal neurons. In addition, we show that the release of ATP under hypoxia is able to inhibit LTD by acting on postsynaptic P2Y(1) receptors. In conclusion, these data suggest that the reduction of Ca(2+) influx via VSCCs caused by the activation of P2Y(1) receptors by ATP is the possible mechanism for the inhibition of LTD in prefrontal cortex. acknowledgement: " The financial support of the Deutsche Forschungsgemeinschaft (IL 20/12-1, KI 677/2-4) is gratefully acknowledged.\r\nWe thank B. H. Koller (Department of Genetics and Molecular Biology, University of North Carolina at Chapel Hill, NC, USA) for the generous supply of P2Y1−/− and P2Y2−/− mice. We are grateful to Dr. A. Schulz for reanalysing the genotype of the P2Y1−/− mice. The authors thank P. Jonas and U. Heinemann for many helpful comments and A-K. Krause, L Feige and M. Eberts for their excellent technical support." author: - first_name: José full_name: Guzmán, José id: 30CC5506-F248-11E8-B48F-1D18A9856A87 last_name: Guzmán - first_name: Hartmut full_name: Schmidt, Hartmut last_name: Schmidt - first_name: Heike full_name: Franke, Heike last_name: Franke - first_name: Ute full_name: Krügel, Ute last_name: Krügel - first_name: Jens full_name: Eilers, Jens last_name: Eilers - first_name: Peter full_name: Illes, Peter last_name: Illes - first_name: Zoltan full_name: Gerevich, Zoltan last_name: Gerevich citation: ama: Guzmán J, Schmidt H, Franke H, et al. P2Y1 receptors inhibit long-term depression in the prefrontal cortex. Neuropharmacology. 2010;59(6):406-415. doi:10.1016/j.neuropharm.2010.05.013 apa: Guzmán, J., Schmidt, H., Franke, H., Krügel, U., Eilers, J., Illes, P., & Gerevich, Z. (2010). P2Y1 receptors inhibit long-term depression in the prefrontal cortex. Neuropharmacology. Elsevier. https://doi.org/10.1016/j.neuropharm.2010.05.013 chicago: Guzmán, José, Hartmut Schmidt, Heike Franke, Ute Krügel, Jens Eilers, Peter Illes, and Zoltan Gerevich. “P2Y1 Receptors Inhibit Long-Term Depression in the Prefrontal Cortex.” Neuropharmacology. Elsevier, 2010. https://doi.org/10.1016/j.neuropharm.2010.05.013. ieee: J. Guzmán et al., “P2Y1 receptors inhibit long-term depression in the prefrontal cortex.,” Neuropharmacology, vol. 59, no. 6. Elsevier, pp. 406–415, 2010. ista: Guzmán J, Schmidt H, Franke H, Krügel U, Eilers J, Illes P, Gerevich Z. 2010. P2Y1 receptors inhibit long-term depression in the prefrontal cortex. Neuropharmacology. 59(6), 406–415. mla: Guzmán, José, et al. “P2Y1 Receptors Inhibit Long-Term Depression in the Prefrontal Cortex.” Neuropharmacology, vol. 59, no. 6, Elsevier, 2010, pp. 406–15, doi:10.1016/j.neuropharm.2010.05.013. short: J. Guzmán, H. Schmidt, H. Franke, U. Krügel, J. Eilers, P. Illes, Z. Gerevich, Neuropharmacology 59 (2010) 406–415. date_created: 2018-12-11T12:04:47Z date_published: 2010-11-01T00:00:00Z date_updated: 2021-01-12T07:51:42Z day: '01' department: - _id: PeJo doi: 10.1016/j.neuropharm.2010.05.013 intvolume: ' 59' issue: '6' language: - iso: eng month: '11' oa_version: None page: 406 - 415 publication: Neuropharmacology publication_status: published publisher: Elsevier publist_id: '2512' quality_controlled: '1' scopus_import: 1 status: public title: P2Y1 receptors inhibit long-term depression in the prefrontal cortex. type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 59 year: '2010' ... --- _id: '3832' abstract: - lang: eng text: A recent paper by von Engelhardt et al. identifies a novel auxiliary subunit of native AMPARs, termedCKAMP44. Unlike other auxiliary subunits, CKAMP44 accelerates desensitization and prolongs recovery from desensitization. CKAMP44 is highly expressed in hippocampal dentate gyrus granule cells and decreases the paired-pulse ratio at perforant path input synapses. Thus, both principal and auxiliary AMPAR subunits control the time course of signaling at glutamatergic synapses. article_processing_charge: No author: - first_name: José full_name: Guzmán, José id: 30CC5506-F248-11E8-B48F-1D18A9856A87 last_name: Guzmán - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: 'Guzmán J, Jonas PM. Beyond TARPs: The growing list of auxiliary AMPAR subunits. Neuron. 2010;66(1):8-10. doi:10.1016/j.neuron.2010.04.003' apa: 'Guzmán, J., & Jonas, P. M. (2010). Beyond TARPs: The growing list of auxiliary AMPAR subunits. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2010.04.003' chicago: 'Guzmán, José, and Peter M Jonas. “Beyond TARPs: The Growing List of Auxiliary AMPAR Subunits.” Neuron. Elsevier, 2010. https://doi.org/10.1016/j.neuron.2010.04.003.' ieee: 'J. Guzmán and P. M. Jonas, “Beyond TARPs: The growing list of auxiliary AMPAR subunits,” Neuron, vol. 66, no. 1. Elsevier, pp. 8–10, 2010.' ista: 'Guzmán J, Jonas PM. 2010. Beyond TARPs: The growing list of auxiliary AMPAR subunits. Neuron. 66(1), 8–10.' mla: 'Guzmán, José, and Peter M. Jonas. “Beyond TARPs: The Growing List of Auxiliary AMPAR Subunits.” Neuron, vol. 66, no. 1, Elsevier, 2010, pp. 8–10, doi:10.1016/j.neuron.2010.04.003.' short: J. Guzmán, P.M. Jonas, Neuron 66 (2010) 8–10. date_created: 2018-12-11T12:05:25Z date_published: 2010-04-15T00:00:00Z date_updated: 2021-01-12T07:52:31Z day: '15' department: - _id: PeJo doi: 10.1016/j.neuron.2010.04.003 external_id: pmid: - '20399724' intvolume: ' 66' issue: '1' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pubmed/20399724 month: '04' oa: 1 oa_version: Published Version page: 8 - 10 pmid: 1 publication: Neuron publication_status: published publisher: Elsevier publist_id: '2377' quality_controlled: '1' scopus_import: 1 status: public title: 'Beyond TARPs: The growing list of auxiliary AMPAR subunits' type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 66 year: '2010' ... --- _id: '3833' article_processing_charge: No author: - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 - first_name: Stefan full_name: Hefft, Stefan last_name: Hefft citation: ama: 'Jonas PM, Hefft S. GABA release at terminals of CCK-interneurons: synchrony, asynchrony and modulation by cannabinoid receptors (commentary on Ali & Todorova). The European Journal of Neuroscience. 2010;31(7):1194-1195. doi:10.1111/j.1460-9568.2010.07189.x' apa: 'Jonas, P. M., & Hefft, S. (2010). GABA release at terminals of CCK-interneurons: synchrony, asynchrony and modulation by cannabinoid receptors (commentary on Ali & Todorova). The European Journal of Neuroscience. Wiley-Blackwell. https://doi.org/10.1111/j.1460-9568.2010.07189.x' chicago: 'Jonas, Peter M, and Stefan Hefft. “GABA Release at Terminals of CCK-Interneurons: Synchrony, Asynchrony and Modulation by Cannabinoid Receptors (Commentary on Ali & Todorova).” The European Journal of Neuroscience. Wiley-Blackwell, 2010. https://doi.org/10.1111/j.1460-9568.2010.07189.x.' ieee: 'P. M. Jonas and S. Hefft, “GABA release at terminals of CCK-interneurons: synchrony, asynchrony and modulation by cannabinoid receptors (commentary on Ali & Todorova),” The European Journal of Neuroscience, vol. 31, no. 7. Wiley-Blackwell, pp. 1194–1195, 2010.' ista: 'Jonas PM, Hefft S. 2010. GABA release at terminals of CCK-interneurons: synchrony, asynchrony and modulation by cannabinoid receptors (commentary on Ali & Todorova). The European Journal of Neuroscience. 31(7), 1194–1195.' mla: 'Jonas, Peter M., and Stefan Hefft. “GABA Release at Terminals of CCK-Interneurons: Synchrony, Asynchrony and Modulation by Cannabinoid Receptors (Commentary on Ali & Todorova).” The European Journal of Neuroscience, vol. 31, no. 7, Wiley-Blackwell, 2010, pp. 1194–95, doi:10.1111/j.1460-9568.2010.07189.x.' short: P.M. Jonas, S. Hefft, The European Journal of Neuroscience 31 (2010) 1194–1195. date_created: 2018-12-11T12:05:25Z date_published: 2010-03-19T00:00:00Z date_updated: 2021-01-12T07:52:31Z day: '19' department: - _id: PeJo doi: 10.1111/j.1460-9568.2010.07189.x intvolume: ' 31' issue: '7' language: - iso: eng month: '03' oa_version: None page: 1194 - 1195 publication: The European Journal of Neuroscience publication_status: published publisher: Wiley-Blackwell publist_id: '2378' quality_controlled: '1' scopus_import: 1 status: public title: 'GABA release at terminals of CCK-interneurons: synchrony, asynchrony and modulation by cannabinoid receptors (commentary on Ali & Todorova)' type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 31 year: '2010' ...