--- _id: '320' abstract: - lang: eng text: 'Fast-spiking, parvalbumin-expressing GABAergic interneurons (PV+-BCs) express a complex machinery of rapid signaling mechanisms, including specialized voltage-gated ion channels to generate brief action potentials (APs). However, short APs are associated with overlapping Na+ and K+ fluxes and are therefore energetically expensive. How the potentially vicious combination of high AP frequency and inefficient spike generation can be reconciled with limited energy supply is presently unclear. To address this question, we performed direct recordings from the PV+-BC axon, the subcellular structure where active conductances for AP initiation and propagation are located. Surprisingly, the energy required for the AP was, on average, only ∼1.6 times the theoretical minimum. High energy efficiency emerged from the combination of fast inactivation of Na+ channels and delayed activation of Kv3-type K+ channels, which minimized ion flux overlap during APs. Thus, the complementary tuning of axonal Na+ and K+ channel gating optimizes both fast signaling properties and metabolic efficiency. Hu et al. demonstrate that action potentials in parvalbumin-expressing GABAergic interneuron axons are energetically efficient, which is highly unexpected given their brief duration. High energy efficiency emerges from the combination of fast inactivation of voltage-gated Na+ channels and delayed activation of Kv3 channels in the axon. ' article_processing_charge: Yes (in subscription journal) author: - first_name: Hua full_name: Hu, Hua id: 4AC0145C-F248-11E8-B48F-1D18A9856A87 last_name: Hu - first_name: Fabian full_name: Roth, Fabian last_name: Roth - 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: 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, Roth F, Vandael DH, Jonas PM. Complementary tuning of Na+ and K+ channel gating underlies fast and energy-efficient action potentials in GABAergic interneuron axons. Neuron. 2018;98(1):156-165. doi:10.1016/j.neuron.2018.02.024 apa: Hu, H., Roth, F., Vandael, D. H., & Jonas, P. M. (2018). Complementary tuning of Na+ and K+ channel gating underlies fast and energy-efficient action potentials in GABAergic interneuron axons. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2018.02.024 chicago: Hu, Hua, Fabian Roth, David H Vandael, and Peter M Jonas. “Complementary Tuning of Na+ and K+ Channel Gating Underlies Fast and Energy-Efficient Action Potentials in GABAergic Interneuron Axons.” Neuron. Elsevier, 2018. https://doi.org/10.1016/j.neuron.2018.02.024. ieee: H. Hu, F. Roth, D. H. Vandael, and P. M. Jonas, “Complementary tuning of Na+ and K+ channel gating underlies fast and energy-efficient action potentials in GABAergic interneuron axons,” Neuron, vol. 98, no. 1. Elsevier, pp. 156–165, 2018. ista: Hu H, Roth F, Vandael DH, Jonas PM. 2018. Complementary tuning of Na+ and K+ channel gating underlies fast and energy-efficient action potentials in GABAergic interneuron axons. Neuron. 98(1), 156–165. mla: Hu, Hua, et al. “Complementary Tuning of Na+ and K+ Channel Gating Underlies Fast and Energy-Efficient Action Potentials in GABAergic Interneuron Axons.” Neuron, vol. 98, no. 1, Elsevier, 2018, pp. 156–65, doi:10.1016/j.neuron.2018.02.024. short: H. Hu, F. Roth, D.H. Vandael, P.M. Jonas, Neuron 98 (2018) 156–165. corr_author: '1' date_created: 2018-12-11T11:45:48Z date_published: 2018-04-04T00:00:00Z date_updated: 2025-04-15T08:29:04Z day: '04' ddc: - '570' department: - _id: PeJo doi: 10.1016/j.neuron.2018.02.024 ec_funded: 1 external_id: isi: - '000429192100016' file: - access_level: open_access checksum: 76070f3729f9c603e1080d0151aa2b11 content_type: application/pdf creator: dernst date_created: 2018-12-17T10:37:50Z date_updated: 2020-07-14T12:46:03Z file_id: '5690' file_name: 2018_Neuron_Hu.pdf file_size: 3180444 relation: main_file file_date_updated: 2020-07-14T12:46:03Z fulldoi: https://doi.org/10.1016/j.neuron.2018.02.024 has_accepted_license: '1' intvolume: ' 98' isi: 1 issue: '1' language: - iso: eng license: https://creativecommons.org/licenses/by/4.0/ month: '04' oa: 1 oa_version: Published Version page: 156 - 165 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 glutamatergic synapse - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses - _id: 25C5A090-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Z00312 name: Synaptic communication in neuronal microcircuits publication: Neuron publication_status: published publisher: Elsevier publist_id: '7545' quality_controlled: '1' related_material: link: - description: News on IST Homepage relation: press_release url: https://ist.ac.at/en/news/a-certain-type-of-neurons-is-more-energy-efficient-than-previously-assumed/ scopus_import: '1' status: public title: Complementary tuning of Na+ and K+ channel gating underlies fast and energy-efficient action potentials in GABAergic interneuron axons 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: 98 year: '2018' ... --- OA_place: publisher _id: '324' abstract: - lang: eng text: Neuronal networks in the brain consist of two main types of neuron, glutamatergic principal neurons and GABAergic interneurons. Although these interneurons only represent 10–20% of the whole population, they mediate feedback and feedforward inhibition and are involved in the generation of high-frequency network oscillations. A hallmark functional property of GABAergic interneurons, especially of the parvalbumin‑expressing (PV+) subtypes, is the speed of signaling at their output synapse across species and brain regions. Several molecular and subcellular factors may underlie the submillisecond signaling at GABAergic synapses. Such as the selective use of P/Q type Ca2+ channels and the tight coupling between Ca2+ channels and Ca2+ sensors of exocytosis. However, whether the molecular identity of the release sensor contributes to these signaling properties remains unclear. Besides, these interneurons are mainly show depression in response to train of stimuli. How could they keep sufficient release to control the activity of postsynaptic principal neurons during high network activity, is largely elusive. For my Ph.D. work, we firstly examined the Ca2+ sensor of exocytosis at the GABAergic basket cell (BC) to Purkinje cell (PC) synapse in the 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% compared to the wild-type control, identifying Syt2 as the major Ca2+ sensor at BC‑PC synapses. Differential adenovirus-mediated rescue revealed 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 the release sensor at BC–PC synapse ensures fast feedforward inhibition in cerebellar microcircuits. Additionally, we tested the function of another synaptotagmin member, Syt7, for inhibitory synaptic transmission at the BC–PC synapse. Syt7 is thought to be a Ca2+ sensor that mediates asynchronous transmitter release and facilitation at synapses. However, it is strongly expressed in fast-spiking, PV+ GABAergic interneurons and the output synapses of these neurons produce only minimal asynchronous release and show depression rather than facilitation. How could Syt7, a facilitation sensor, contribute to the depressed inhibitory synaptic transmission needs to be further investigated and understood. Our results indicated 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. Taken together, our results confirmed that Syt2, which has the fastest kinetic properties among all synaptotagmin members, is mainly used by the inhibitory BC‑PC synapse for synaptic transmission, contributing to the speed and temporal precision of transmitter release. Furthermore, we showed that Syt7, another highly expressed synaptotagmin member in the output synapses of cerebellar BCs, is used for ensuring efficient inhibitor synaptic transmission during high activity. alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Chong full_name: Chen, Chong id: 3DFD581A-F248-11E8-B48F-1D18A9856A87 last_name: Chen citation: ama: Chen C. Synaptotagmins ensure speed and efficiency of inhibitory neurotransmitter release. 2018. doi:10.15479/AT:ISTA:th_997 apa: Chen, C. (2018). Synaptotagmins ensure speed and efficiency of inhibitory neurotransmitter release. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th_997 chicago: Chen, Chong. “Synaptotagmins Ensure Speed and Efficiency of Inhibitory Neurotransmitter Release.” Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th_997. ieee: C. Chen, “Synaptotagmins ensure speed and efficiency of inhibitory neurotransmitter release,” Institute of Science and Technology Austria, 2018. ista: Chen C. 2018. Synaptotagmins ensure speed and efficiency of inhibitory neurotransmitter release. Institute of Science and Technology Austria. mla: Chen, Chong. Synaptotagmins Ensure Speed and Efficiency of Inhibitory Neurotransmitter Release. Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:th_997. short: C. Chen, Synaptotagmins Ensure Speed and Efficiency of Inhibitory Neurotransmitter Release, Institute of Science and Technology Austria, 2018. corr_author: '1' date_created: 2018-12-11T11:45:49Z date_published: 2018-03-01T00:00:00Z date_updated: 2026-04-08T14:09:29Z day: '01' ddc: - '571' degree_awarded: PhD department: - _id: PeJo doi: 10.15479/AT:ISTA:th_997 file: - access_level: open_access checksum: 8e163ae9e927401b9fa7c1b3e6a3631a content_type: application/pdf creator: system date_created: 2018-12-12T10:13:58Z date_updated: 2020-07-14T12:46:04Z file_id: '5046' file_name: IST-2018-997-v1+1_Thesis_chong_a.pdf file_size: 8719458 relation: main_file - access_level: closed checksum: f7d7260029a5fbb5c982db61328ade52 content_type: application/octet-stream creator: dernst date_created: 2019-04-05T09:25:26Z date_updated: 2020-07-14T12:46:04Z file_id: '6221' file_name: 2018_Thesis_chong_source.pages file_size: 47841940 relation: source_file file_date_updated: 2020-07-14T12:46:04Z fulldoi: https://doi.org/10.15479/AT:ISTA:th_997 has_accepted_license: '1' language: - iso: eng month: '03' oa: 1 oa_version: Published Version page: '110' publication_identifier: issn: - 2663-337X publication_status: published publisher: Institute of Science and Technology Austria publist_id: '7541' pubrep_id: '997' related_material: record: - id: '1117' relation: part_of_dissertation status: public - id: '749' 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: Synaptotagmins ensure speed and efficiency of inhibitory neurotransmitter release 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: dissertation user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd year: '2018' ... --- _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 orcid: 0000-0003-0256-6529 - 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: 2026-10-27T23:30:30Z 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 fulldoi: https://doi.org/10.1038/s41467-018-06899-3 has_accepted_license: '1' intvolume: ' 9' isi: 1 issue: '1' language: - iso: eng 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 glutamatergic synapse - _id: 25C5A090-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Z00312 name: Synaptic communication in neuronal microcircuits 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: '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: 2026-04-08T14:09:28Z 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 fulldoi: https://doi.org/10.1016/j.celrep.2016.12.067 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: - 2211-1247 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: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 18 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: 2025-04-15T07:20:01Z 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 fulldoi: https://doi.org/10.1016/j.neuron.2016.12.018 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: '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 article_processing_charge: No 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: 2025-09-11T07:27:53Z day: '01' ddc: - '005' department: - _id: ScienComp - _id: PeJo doi: 10.3233/978-1-61499-759-7-356 external_id: isi: - '000426828000047' 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 fulldoi: https://doi.org/10.3233/978-1-61499-759-7-356 has_accepted_license: '1' intvolume: ' 236' isi: 1 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: 317138e5-6ab7-11ef-aa6d-ffef3953e345 volume: 236 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: 2025-07-10T11:54:59Z 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 fulldoi: https://doi.org/10.1038/s41467-017-00936-3 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: - 2041-1723 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: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 8 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. article_processing_charge: No 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: 2025-09-10T11:06:14Z day: '01' department: - _id: PeJo doi: 10.1111/gtc.12508 external_id: isi: - '000409224300003' fulldoi: https://doi.org/10.1111/gtc.12508 intvolume: ' 22' isi: 1 issue: '8' language: - iso: eng month: '08' oa_version: None page: 715 - 722 publication: Genes to Cells publication_identifier: issn: - 1356-9597 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: 317138e5-6ab7-11ef-aa6d-ffef3953e345 volume: 22 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. corr_author: '1' date_created: 2018-12-11T11:48:18Z date_published: 2017-11-21T00:00:00Z date_updated: 2026-04-08T14:09:28Z 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 fulldoi: https://doi.org/10.1016/j.celrep.2017.10.122 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 glutamatergic synapse publication: Cell Reports publication_identifier: issn: - 2211-1247 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: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 21 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: 2026-04-16T10:05:51Z day: '17' department: - _id: PeJo doi: 10.1016/j.neuron.2017.05.011 external_id: isi: - '000401415100002' fulldoi: https://doi.org/10.1016/j.neuron.2017.05.011 intvolume: ' 94' isi: 1 issue: '4' language: - iso: eng month: '05' oa_version: None page: 694 - 696 publication: Neuron publication_identifier: issn: - 0896-6273 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: ba8df636-2132-11f1-aed0-ed93e2281fdd volume: 94 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).' article_processing_charge: No 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: 2025-09-22T14:10:50Z day: '01' department: - _id: MiSi - _id: PeJo doi: 10.1038/ni.3590 external_id: isi: - '000388056400006' fulldoi: https://doi.org/10.1038/ni.3590 intvolume: ' 17' isi: 1 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: 317138e5-6ab7-11ef-aa6d-ffef3953e345 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 article_processing_charge: No 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). corr_author: '1' date_created: 2018-12-11T11:51:22Z date_published: 2016-10-25T00:00:00Z date_updated: 2025-09-22T08:26:29Z day: '25' ddc: - '571' - '572' department: - _id: PeJo doi: 10.7554/eLife.17977 ec_funded: 1 external_id: isi: - '000387034600001' 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 fulldoi: https://doi.org/10.7554/eLife.17977 has_accepted_license: '1' intvolume: ' 5' isi: 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 - _id: 25B7EB9E-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '692692' name: Biophysics and circuit function of a giant cortical glutamatergic 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: 317138e5-6ab7-11ef-aa6d-ffef3953e345 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 article_processing_charge: No author: - first_name: José full_name: Guzmán, José id: 30CC5506-F248-11E8-B48F-1D18A9856A87 last_name: Guzmán orcid: 0000-0003-2209-5242 - 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. corr_author: '1' date_created: 2018-12-11T11:51:31Z date_published: 2016-09-09T00:00:00Z date_updated: 2025-09-22T08:12:10Z day: '09' ddc: - '570' department: - _id: ScienComp - _id: PeJo doi: 10.1126/science.aaf1836 ec_funded: 1 external_id: isi: - '000382626800045' 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 fulldoi: https://doi.org/10.1126/science.aaf1836 has_accepted_license: '1' intvolume: ' 353' isi: 1 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: 317138e5-6ab7-11ef-aa6d-ffef3953e345 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' article_processing_charge: No author: - first_name: José full_name: Guzmán, José id: 30CC5506-F248-11E8-B48F-1D18A9856A87 last_name: Guzmán orcid: 0000-0003-2209-5242 - 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: 2025-09-18T11:45:18Z day: '01' ddc: - '570' department: - _id: PeJo doi: 10.1155/2016/1207393 external_id: isi: - '000374056200001' 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 fulldoi: https://doi.org/10.1155/2016/1207393 has_accepted_license: '1' intvolume: ' 2016' isi: 1 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: 317138e5-6ab7-11ef-aa6d-ffef3953e345 volume: 2016 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. corr_author: '1' date_created: 2018-12-11T11:53:03Z date_published: 2016-05-01T00:00:00Z date_updated: 2025-09-18T10:58:31Z day: '01' ddc: - '570' department: - _id: PeJo doi: 10.1002/hipo.22550 external_id: isi: - '000374666700011' 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 fulldoi: https://doi.org/10.1002/hipo.22550 has_accepted_license: '1' intvolume: ' 26' isi: 1 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: 317138e5-6ab7-11ef-aa6d-ffef3953e345 volume: 26 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' article_processing_charge: No 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). corr_author: '1' date_created: 2018-12-11T11:51:59Z date_published: 2016-05-13T00:00:00Z date_updated: 2026-07-29T11:31:52Z day: '13' ddc: - '570' department: - _id: PeJo doi: 10.1038/ncomms11552 ec_funded: 1 external_id: isi: - '000375938200001' 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 fulldoi: https://doi.org/10.1038/ncomms11552 has_accepted_license: '1' intvolume: ' 7' isi: 1 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: 317138e5-6ab7-11ef-aa6d-ffef3953e345 volume: 7 year: '2016' ... --- OA_place: publisher _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. corr_author: '1' date_created: 2018-12-11T11:51:46Z date_published: 2016-03-01T00:00:00Z date_updated: 2026-07-29T11:31:52Z day: '01' ddc: - '570' degree_awarded: PhD department: - _id: PeJo - _id: GradSch doi_confirm: '1' 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: 8b945eb4-e2f2-11eb-945a-df72226e66a9 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 corr_author: '1' date_created: 2023-05-05T12:54:47Z date_published: 2016-02-24T00:00:00Z date_updated: 2026-10-14T09:40:16Z 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://asc.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: '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: 2025-09-23T08:12:18Z day: '01' department: - _id: PeJo doi: 10.2174/1874467208666150507105443 external_id: isi: - '000217186100005' pmid: - '25966692' fulldoi: https://doi.org/10.2174/1874467208666150507105443 intvolume: ' 8' isi: 1 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: 317138e5-6ab7-11ef-aa6d-ffef3953e345 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." article_processing_charge: No 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: 2025-09-23T08:30:00Z day: '15' department: - _id: PeJo doi: 10.1113/JP271078 external_id: isi: - '000365267700003' pmid: - '26282459' fulldoi: https://doi.org/10.1113/JP271078 intvolume: ' 593' isi: 1 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: 317138e5-6ab7-11ef-aa6d-ffef3953e345 volume: 593 year: '2015' ...