--- _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 has_accepted_license: '1' intvolume: ' 5' isi: 1 language: - iso: eng license: https://creativecommons.org/licenses/by/4.0/ 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 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 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 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 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: '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' 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' 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' ... --- _id: '1580' abstract: - lang: eng text: Synapsins (Syns) are an evolutionarily conserved family of presynaptic proteins crucial for the fine-tuning of synaptic function. A large amount of experimental evidences has shown that Syns are involved in the development of epileptic phenotypes and several mutations in Syn genes have been associated with epilepsy in humans and animal models. Syn mutations induce alterations in circuitry and neurotransmitter release, differentially affecting excitatory and inhibitory synapses, thus causing an excitation/inhibition imbalance in network excitability toward hyperexcitability that may be a determinant with regard to the development of epilepsy. Another approach to investigate epileptogenic mechanisms is to understand how silencing Syn affects the cellular behavior of single neurons and is associated with the hyperexcitable phenotypes observed in epilepsy. Here, we examined the functional effects of antisense-RNA inhibition of Syn expression on individually identified and isolated serotonergic cells of the Helix land snail. We found that Helix synapsin silencing increases cell excitability characterized by a slightly depolarized resting membrane potential, decreases the rheobase, reduces the threshold for action potential (AP) firing and increases the mean and instantaneous firing rates, with respect to control cells. The observed increase of Ca2+ and BK currents in Syn-silenced cells seems to be related to changes in the shape of the AP waveform. These currents sustain the faster spiking in Syn-deficient cells by increasing the after hyperpolarization and limiting the Na+ and Ca2+ channel inactivation during repetitive firing. This in turn speeds up the depolarization phase by reaching the AP threshold faster. Our results provide evidence that Syn silencing increases intrinsic cell excitability associated with increased Ca2+ and Ca2+-dependent BK currents in the absence of excitatory or inhibitory inputs. article_processing_charge: No article_type: original author: - first_name: Oscar full_name: Brenes, Oscar last_name: Brenes - first_name: David H full_name: Vandael, David H id: 3AE48E0A-F248-11E8-B48F-1D18A9856A87 last_name: Vandael orcid: 0000-0001-7577-1676 - first_name: Emilio full_name: Carbone, Emilio last_name: Carbone - first_name: Pier full_name: Montarolo, Pier last_name: Montarolo - first_name: Mirella full_name: Ghirardi, Mirella last_name: Ghirardi citation: ama: Brenes O, Vandael DH, Carbone E, Montarolo P, Ghirardi M. Knock-down of synapsin alters cell excitability and action potential waveform by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons. Neuroscience. 2015;311:430-443. doi:10.1016/j.neuroscience.2015.10.046 apa: Brenes, O., Vandael, D. H., Carbone, E., Montarolo, P., & Ghirardi, M. (2015). Knock-down of synapsin alters cell excitability and action potential waveform by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons. Neuroscience. Elsevier. https://doi.org/10.1016/j.neuroscience.2015.10.046 chicago: Brenes, Oscar, David H Vandael, Emilio Carbone, Pier Montarolo, and Mirella Ghirardi. “Knock-down of Synapsin Alters Cell Excitability and Action Potential Waveform by Potentiating BK and Voltage Gated Ca2 Currents in Helix Serotonergic Neurons.” Neuroscience. Elsevier, 2015. https://doi.org/10.1016/j.neuroscience.2015.10.046. ieee: O. Brenes, D. H. Vandael, E. Carbone, P. Montarolo, and M. Ghirardi, “Knock-down of synapsin alters cell excitability and action potential waveform by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons,” Neuroscience, vol. 311. Elsevier, pp. 430–443, 2015. ista: Brenes O, Vandael DH, Carbone E, Montarolo P, Ghirardi M. 2015. Knock-down of synapsin alters cell excitability and action potential waveform by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons. Neuroscience. 311, 430–443. mla: Brenes, Oscar, et al. “Knock-down of Synapsin Alters Cell Excitability and Action Potential Waveform by Potentiating BK and Voltage Gated Ca2 Currents in Helix Serotonergic Neurons.” Neuroscience, vol. 311, Elsevier, 2015, pp. 430–43, doi:10.1016/j.neuroscience.2015.10.046. short: O. Brenes, D.H. Vandael, E. Carbone, P. Montarolo, M. Ghirardi, Neuroscience 311 (2015) 430–443. date_created: 2018-12-11T11:52:50Z date_published: 2015-12-17T00:00:00Z date_updated: 2025-09-23T09:25:46Z day: '17' ddc: - '570' department: - _id: PeJo doi: 10.1016/j.neuroscience.2015.10.046 external_id: isi: - '000366144000037' file: - access_level: open_access checksum: af2c4c994718c7be417eba0dc746aac9 content_type: application/pdf creator: dernst date_created: 2020-05-15T06:50:20Z date_updated: 2020-07-14T12:45:02Z file_id: '7849' file_name: 2015_Neuroscience_Brenes.pdf file_size: 5563015 relation: main_file file_date_updated: 2020-07-14T12:45:02Z has_accepted_license: '1' intvolume: ' 311' isi: 1 language: - iso: eng month: '12' oa: 1 oa_version: Submitted Version page: 430 - 443 publication: Neuroscience publication_status: published publisher: Elsevier publist_id: '5591' quality_controlled: '1' scopus_import: '1' status: public title: Knock-down of synapsin alters cell excitability and action potential waveform by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345 volume: 311 year: '2015' ... --- _id: '1614' abstract: - lang: eng text: 'GABAergic perisoma-inhibiting fast-spiking interneurons (PIIs) effectively control the activity of large neuron populations by their wide axonal arborizations. It is generally assumed that the output of one PII to its target cells is strong and rapid. Here, we show that, unexpectedly, both strength and time course of PII-mediated perisomatic inhibition change with distance between synaptically connected partners in the rodent hippocampus. Synaptic signals become weaker due to lower contact numbers and decay more slowly with distance, very likely resulting from changes in GABAA receptor subunit composition. When distance-dependent synaptic inhibition is introduced to a rhythmically active neuronal network model, randomly driven principal cell assemblies are strongly synchronized by the PIIs, leading to higher precision in principal cell spike times than in a network with uniform synaptic inhibition. ' article_processing_charge: No author: - first_name: Michael full_name: Strüber, Michael last_name: Strüber - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 - first_name: Marlene full_name: Bartos, Marlene last_name: Bartos citation: ama: Strüber M, Jonas PM, Bartos M. Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells. PNAS. 2015;112(4):1220-1225. doi:10.1073/pnas.1412996112 apa: Strüber, M., Jonas, P. M., & Bartos, M. (2015). Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1412996112 chicago: Strüber, Michael, Peter M Jonas, and Marlene Bartos. “Strength and Duration of Perisomatic GABAergic Inhibition Depend on Distance between Synaptically Connected Cells.” PNAS. National Academy of Sciences, 2015. https://doi.org/10.1073/pnas.1412996112. ieee: M. Strüber, P. M. Jonas, and M. Bartos, “Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells,” PNAS, vol. 112, no. 4. National Academy of Sciences, pp. 1220–1225, 2015. ista: Strüber M, Jonas PM, Bartos M. 2015. Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells. PNAS. 112(4), 1220–1225. mla: Strüber, Michael, et al. “Strength and Duration of Perisomatic GABAergic Inhibition Depend on Distance between Synaptically Connected Cells.” PNAS, vol. 112, no. 4, National Academy of Sciences, 2015, pp. 1220–25, doi:10.1073/pnas.1412996112. short: M. Strüber, P.M. Jonas, M. Bartos, PNAS 112 (2015) 1220–1225. date_created: 2018-12-11T11:53:02Z date_published: 2015-01-27T00:00:00Z date_updated: 2025-09-23T10:49:39Z day: '27' ddc: - '570' department: - _id: PeJo doi: 10.1073/pnas.1412996112 ec_funded: 1 external_id: isi: - '000348417000066' pmid: - '25583495' file: - access_level: open_access checksum: 6703309a1f58493cf5a704211fb6ebed content_type: application/pdf creator: dernst date_created: 2019-01-17T07:52:40Z date_updated: 2020-07-14T12:45:07Z file_id: '5838' file_name: 2015_PNAS_Strueber.pdf file_size: 1280860 relation: main_file file_date_updated: 2020-07-14T12:45:07Z has_accepted_license: '1' intvolume: ' 112' isi: 1 issue: '4' language: - iso: eng month: '01' oa: 1 oa_version: Published Version page: 1220 - 1225 pmid: 1 project: - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons publication: PNAS publication_status: published publisher: National Academy of Sciences publist_id: '5552' quality_controlled: '1' scopus_import: '1' status: public title: Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells type: journal_article user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345 volume: 112 year: '2015' ... --- _id: '1615' abstract: - lang: eng text: Loss-of-function mutations in the synaptic adhesion protein Neuroligin-4 are among the most common genetic abnormalities associated with autism spectrum disorders, but little is known about the function of Neuroligin-4 and the consequences of its loss. We assessed synaptic and network characteristics in Neuroligin-4 knockout mice, focusing on the hippocampus as a model brain region with a critical role in cognition and memory, and found that Neuroligin-4 deletion causes subtle defects of the protein composition and function of GABAergic synapses in the hippocampal CA3 region. Interestingly, these subtle synaptic changes are accompanied by pronounced perturbations of γ-oscillatory network activity, which has been implicated in cognitive function and is altered in multiple psychiatric and neurodevelopmental disorders. Our data provide important insights into the mechanisms by which Neuroligin-4-dependent GABAergic synapses may contribute to autism phenotypes and indicate new strategies for therapeutic approaches. acknowledgement: This work was supported by the Max Planck Society (N.B. and H.E.), the European Commission (EU-AIMS FP7-115300, N.B. and H.E.; Marie Curie IRG, D.K.-B.), the German Research Foundation (CNMPB, N.B., H.E., and F.V.), the Alexander von Humboldt-Foundation (D.K.-B.), and the Austrian Fond zur Förderung der Wissenschaftlichen Forschung (P 24909-B24, P.J.). M.H. was a student of the doctoral program Molecular Physiology of the Brain. Dr. J.-M. Fritschy generously provided the GABAARγ2 antibody. We thank F. Benseler, I. Thanhäuser, D. Schwerdtfeger, A. Ronnenberg, and D. Winkler for valuable advice and excellent technical support. We are grateful to the staff at the animal facility of the Max Planck Institute of Experimental Medicine for mouse husbandry. article_processing_charge: No author: - first_name: Matthieu full_name: Hammer, Matthieu last_name: Hammer - first_name: Dilja full_name: Krueger Burg, Dilja last_name: Krueger Burg - first_name: Liam full_name: Tuffy, Liam last_name: Tuffy - first_name: Benjamin full_name: Cooper, Benjamin last_name: Cooper - first_name: Holger full_name: Taschenberger, Holger last_name: Taschenberger - first_name: Sarit full_name: Goswami, Sarit id: 3A578F32-F248-11E8-B48F-1D18A9856A87 last_name: Goswami - first_name: Hannelore full_name: Ehrenreich, Hannelore last_name: Ehrenreich - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 - first_name: Frederique full_name: Varoqueaux, Frederique last_name: Varoqueaux - first_name: Jeong full_name: Rhee, Jeong last_name: Rhee - first_name: Nils full_name: Brose, Nils last_name: Brose citation: ama: Hammer M, Krueger Burg D, Tuffy L, et al. Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism. Cell Reports. 2015;13(3):516-523. doi:10.1016/j.celrep.2015.09.011 apa: Hammer, M., Krueger Burg, D., Tuffy, L., Cooper, B., Taschenberger, H., Goswami, S., … Brose, N. (2015). Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2015.09.011 chicago: Hammer, Matthieu, Dilja Krueger Burg, Liam Tuffy, Benjamin Cooper, Holger Taschenberger, Sarit Goswami, Hannelore Ehrenreich, et al. “Perturbed Hippocampal Synaptic Inhibition and γ-Oscillations in a Neuroligin-4 Knockout Mouse Model of Autism.” Cell Reports. Cell Press, 2015. https://doi.org/10.1016/j.celrep.2015.09.011. ieee: M. Hammer et al., “Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism,” Cell Reports, vol. 13, no. 3. Cell Press, pp. 516–523, 2015. ista: Hammer M, Krueger Burg D, Tuffy L, Cooper B, Taschenberger H, Goswami S, Ehrenreich H, Jonas PM, Varoqueaux F, Rhee J, Brose N. 2015. Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism. Cell Reports. 13(3), 516–523. mla: Hammer, Matthieu, et al. “Perturbed Hippocampal Synaptic Inhibition and γ-Oscillations in a Neuroligin-4 Knockout Mouse Model of Autism.” Cell Reports, vol. 13, no. 3, Cell Press, 2015, pp. 516–23, doi:10.1016/j.celrep.2015.09.011. short: M. Hammer, D. Krueger Burg, L. Tuffy, B. Cooper, H. Taschenberger, S. Goswami, H. Ehrenreich, P.M. Jonas, F. Varoqueaux, J. Rhee, N. Brose, Cell Reports 13 (2015) 516–523. date_created: 2018-12-11T11:53:02Z date_published: 2015-10-20T00:00:00Z date_updated: 2025-09-23T09:48:31Z day: '20' ddc: - '570' department: - _id: PeJo doi: 10.1016/j.celrep.2015.09.011 external_id: isi: - '000363780000008' file: - access_level: open_access checksum: 44d30fbb543774b076b4938bd36af9d7 content_type: application/pdf creator: system date_created: 2018-12-12T10:13:23Z date_updated: 2020-07-14T12:45:07Z file_id: '5005' file_name: IST-2016-470-v1+1_1-s2.0-S2211124715010220-main.pdf file_size: 2314406 relation: main_file file_date_updated: 2020-07-14T12:45:07Z has_accepted_license: '1' intvolume: ' 13' isi: 1 issue: '3' language: - iso: eng month: '10' oa: 1 oa_version: Published Version page: 516 - 523 publication: Cell Reports publication_status: published publisher: Cell Press publist_id: '5551' pubrep_id: '470' quality_controlled: '1' scopus_import: '1' status: public title: Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345 volume: 13 year: '2015' ... --- _id: '1845' abstract: - lang: eng text: Based on extrapolation from excitatory synapses, it is often assumed that depletion of the releasable pool of synaptic vesicles is the main factor underlying depression at inhibitory synapses. In this issue of Neuron, using subcellular patch-clamp recording from inhibitory presynaptic terminals, Kawaguchi and Sakaba (2015) show that at Purkinje cell-deep cerebellar nuclei neuron synapses, changes in presynaptic action potential waveform substantially contribute to synaptic depression. Based on extrapolation from excitatory synapses, it is often assumed that depletion of the releasable pool of synaptic vesicles is the main factor underlying depression at inhibitory synapses. In this issue of Neuron, using subcellular patch-clamp recording from inhibitory presynaptic terminals, Kawaguchi and Sakaba (2015) show that at Purkinje cell-deep cerebellar nuclei neuron synapses, changes in presynaptic action potential waveform substantially contribute to synaptic depression. article_processing_charge: No author: - first_name: David H full_name: Vandael, David H id: 3AE48E0A-F248-11E8-B48F-1D18A9856A87 last_name: Vandael orcid: 0000-0001-7577-1676 - first_name: 'Claudia ' full_name: 'Espinoza Martinez, Claudia ' id: 31FFEE2E-F248-11E8-B48F-1D18A9856A87 last_name: Espinoza Martinez orcid: 0000-0003-4710-2082 - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Vandael DH, Espinoza Martinez C, Jonas PM. Excitement about inhibitory presynaptic terminals. Neuron. 2015;85(6):1149-1151. doi:10.1016/j.neuron.2015.03.006 apa: Vandael, D. H., Espinoza Martinez, C., & Jonas, P. M. (2015). Excitement about inhibitory presynaptic terminals. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2015.03.006 chicago: Vandael, David H, Claudia Espinoza Martinez, and Peter M Jonas. “Excitement about Inhibitory Presynaptic Terminals.” Neuron. Elsevier, 2015. https://doi.org/10.1016/j.neuron.2015.03.006. ieee: D. H. Vandael, C. Espinoza Martinez, and P. M. Jonas, “Excitement about inhibitory presynaptic terminals,” Neuron, vol. 85, no. 6. Elsevier, pp. 1149–1151, 2015. ista: Vandael DH, Espinoza Martinez C, Jonas PM. 2015. Excitement about inhibitory presynaptic terminals. Neuron. 85(6), 1149–1151. mla: Vandael, David H., et al. “Excitement about Inhibitory Presynaptic Terminals.” Neuron, vol. 85, no. 6, Elsevier, 2015, pp. 1149–51, doi:10.1016/j.neuron.2015.03.006. short: D.H. Vandael, C. Espinoza Martinez, P.M. Jonas, Neuron 85 (2015) 1149–1151. corr_author: '1' date_created: 2018-12-11T11:54:19Z date_published: 2015-03-18T00:00:00Z date_updated: 2025-09-23T08:44:39Z day: '18' ddc: - '570' department: - _id: PeJo doi: 10.1016/j.neuron.2015.03.006 external_id: isi: - '000351319000002' file: - access_level: open_access checksum: d1808550e376a0eca2a950fda017cfa6 content_type: application/pdf creator: system date_created: 2018-12-12T10:16:07Z date_updated: 2020-07-14T12:45:19Z file_id: '5192' file_name: IST-2017-822-v1+1_Perspective_Fig__Final.pdf file_size: 411832 relation: main_file - access_level: open_access checksum: a279f4ae61e6c8f33d68f69a0d02097d content_type: application/pdf creator: system date_created: 2018-12-12T10:16:07Z date_updated: 2020-07-14T12:45:19Z file_id: '5193' file_name: IST-2017-822-v1+2_Perspective_Final2.pdf file_size: 100769 relation: main_file file_date_updated: 2020-07-14T12:45:19Z has_accepted_license: '1' intvolume: ' 85' isi: 1 issue: '6' language: - iso: eng license: https://creativecommons.org/licenses/by-nc/4.0/ month: '03' oa: 1 oa_version: Published Version page: 1149 - 1151 publication: Neuron publication_status: published publisher: Elsevier publist_id: '5256' pubrep_id: '822' quality_controlled: '1' scopus_import: '1' status: public title: Excitement about inhibitory presynaptic terminals tmp: image: /images/cc_by_nc.png legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) short: CC BY-NC (4.0) type: journal_article user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345 volume: 85 year: '2015' ... --- _id: '1834' abstract: - lang: eng text: Huge body of evidences demonstrated that volatile anesthetics affect the hippocampal neurogenesis and neurocognitive functions, and most of them showed impairment at anesthetic dose. Here, we investigated the effect of low dose (1.8%) sevoflurane on hippocampal neurogenesis and dentate gyrus-dependent learning. Neonatal rats at postnatal day 4 to 6 (P4-6) were treated with 1.8% sevoflurane for 6 hours. Neurogenesis was quantified by bromodeoxyuridine labeling and electrophysiology recording. Four and seven weeks after treatment, the Morris water maze and contextual-fear discrimination learning tests were performed to determine the influence on spatial learning and pattern separation. A 6-hour treatment with 1.8% sevoflurane promoted hippocampal neurogenesis and increased the survival of newborn cells and the proportion of immature granular cells in the dentate gyrus of neonatal rats. Sevoflurane-treated rats performed better during the training days of the Morris water maze test and in contextual-fear discrimination learning test. These results suggest that a subanesthetic dose of sevoflurane promotes hippocampal neurogenesis in neonatal rats and facilitates their performance in dentate gyrus-dependent learning tasks. article_processing_charge: No article_type: original author: - first_name: Chong full_name: Chen, Chong id: 3DFD581A-F248-11E8-B48F-1D18A9856A87 last_name: Chen - first_name: Chao full_name: Wang, Chao last_name: Wang - first_name: Xuan full_name: Zhao, Xuan last_name: Zhao - first_name: Tao full_name: Zhou, Tao last_name: Zhou - first_name: Dao full_name: Xu, Dao last_name: Xu - first_name: Zhi full_name: Wang, Zhi last_name: Wang - first_name: Ying full_name: Wang, Ying last_name: Wang citation: ama: Chen C, Wang C, Zhao X, et al. Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats. ASN Neuro. 2015;7(2). doi:10.1177/1759091415575845 apa: Chen, C., Wang, C., Zhao, X., Zhou, T., Xu, D., Wang, Z., & Wang, Y. (2015). Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats. ASN Neuro. SAGE Publications. https://doi.org/10.1177/1759091415575845 chicago: Chen, Chong, Chao Wang, Xuan Zhao, Tao Zhou, Dao Xu, Zhi Wang, and Ying Wang. “Low-Dose Sevoflurane Promoteshippocampal Neurogenesis and Facilitates the Development of Dentate Gyrus-Dependent Learning in Neonatal Rats.” ASN Neuro. SAGE Publications, 2015. https://doi.org/10.1177/1759091415575845. ieee: C. Chen et al., “Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats,” ASN Neuro, vol. 7, no. 2. SAGE Publications, 2015. ista: Chen C, Wang C, Zhao X, Zhou T, Xu D, Wang Z, Wang Y. 2015. Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats. ASN Neuro. 7(2). mla: Chen, Chong, et al. “Low-Dose Sevoflurane Promoteshippocampal Neurogenesis and Facilitates the Development of Dentate Gyrus-Dependent Learning in Neonatal Rats.” ASN Neuro, vol. 7, no. 2, SAGE Publications, 2015, doi:10.1177/1759091415575845. short: C. Chen, C. Wang, X. Zhao, T. Zhou, D. Xu, Z. Wang, Y. Wang, ASN Neuro 7 (2015). date_created: 2018-12-11T11:54:16Z date_published: 2015-04-13T00:00:00Z date_updated: 2025-09-23T09:31:50Z day: '13' ddc: - '570' department: - _id: PeJo doi: 10.1177/1759091415575845 external_id: isi: - '000353223200002' file: - access_level: open_access checksum: 53e16bd3fc2ae2c0d7de9164626c37aa content_type: application/pdf creator: system date_created: 2018-12-12T10:14:08Z date_updated: 2020-07-14T12:45:18Z file_id: '5057' file_name: IST-2016-456-v1+1_ASN_Neuro-2015-Chen-.pdf file_size: 1146814 relation: main_file file_date_updated: 2020-07-14T12:45:18Z has_accepted_license: '1' intvolume: ' 7' isi: 1 issue: '2' language: - iso: eng license: https://creativecommons.org/licenses/by/3.0/ month: '04' oa: 1 oa_version: Published Version publication: ASN Neuro publication_status: published publisher: SAGE Publications publist_id: '5269' pubrep_id: '456' quality_controlled: '1' scopus_import: '1' status: public title: Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/3.0/legalcode name: Creative Commons Attribution 3.0 Unported (CC BY 3.0) short: CC BY (3.0) type: journal_article user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345 volume: 7 year: '2015' ... --- _id: '2228' abstract: - lang: eng text: Fast-spiking, parvalbumin-expressing GABAergic interneurons, a large proportion of which are basket cells (BCs), have a key role in feedforward and feedback inhibition, gamma oscillations and complex information processing. For these functions, fast propagation of action potentials (APs) from the soma to the presynaptic terminals is important. However, the functional properties of interneuron axons remain elusive. We examined interneuron axons by confocally targeted subcellular patch-clamp recording in rat hippocampal slices. APs were initiated in the proximal axon ∼20 μm from the soma and propagated to the distal axon with high reliability and speed. Subcellular mapping revealed a stepwise increase of Na^+ conductance density from the soma to the proximal axon, followed by a further gradual increase in the distal axon. Active cable modeling and experiments with partial channel block revealed that low axonal Na^+ conductance density was sufficient for reliability, but high Na^+ density was necessary for both speed of propagation and fast-spiking AP phenotype. Our results suggest that a supercritical density of Na^+ channels compensates for the morphological properties of interneuron axons (small segmental diameter, extensive branching and high bouton density), ensuring fast AP propagation and high-frequency repetitive firing. article_processing_charge: No author: - first_name: Hua full_name: Hu, Hua id: 4AC0145C-F248-11E8-B48F-1D18A9856A87 last_name: Hu - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Hu H, Jonas PM. A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons. Nature Neuroscience. 2014;17(5):686-693. doi:10.1038/nn.3678 apa: Hu, H., & Jonas, P. M. (2014). A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons. Nature Neuroscience. Nature Publishing Group. https://doi.org/10.1038/nn.3678 chicago: Hu, Hua, and Peter M Jonas. “A Supercritical Density of Na^+ Channels Ensures Fast Signaling in GABAergic Interneuron Axons.” Nature Neuroscience. Nature Publishing Group, 2014. https://doi.org/10.1038/nn.3678. ieee: H. Hu and P. M. Jonas, “A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons,” Nature Neuroscience, vol. 17, no. 5. Nature Publishing Group, pp. 686–693, 2014. ista: Hu H, Jonas PM. 2014. A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons. Nature Neuroscience. 17(5), 686–693. mla: Hu, Hua, and Peter M. Jonas. “A Supercritical Density of Na^+ Channels Ensures Fast Signaling in GABAergic Interneuron Axons.” Nature Neuroscience, vol. 17, no. 5, Nature Publishing Group, 2014, pp. 686–93, doi:10.1038/nn.3678. short: H. Hu, P.M. Jonas, Nature Neuroscience 17 (2014) 686–693. corr_author: '1' date_created: 2018-12-11T11:56:26Z date_published: 2014-03-23T00:00:00Z date_updated: 2025-09-29T11:25:07Z day: '23' department: - _id: PeJo doi: 10.1038/nn.3678 ec_funded: 1 external_id: isi: - '000335016200012' intvolume: ' 17' isi: 1 issue: '5' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4286295/ month: '03' oa: 1 oa_version: Submitted Version page: 686-693 project: - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses publication: Nature Neuroscience publication_identifier: issn: - 1097-6256 publication_status: published publisher: Nature Publishing Group publist_id: '4733' quality_controlled: '1' scopus_import: '1' status: public title: A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons type: journal_article user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345 volume: 17 year: '2014' ... --- _id: '2229' abstract: - lang: eng text: The distance between Ca^2+ channels and release sensors determines the speed and efficacy of synaptic transmission. Tight "nanodomain" channel-sensor coupling initiates transmitter release at synapses in the mature brain, whereas loose "microdomain" coupling appears restricted to early developmental stages. To probe the coupling configuration at a plastic synapse in the mature central nervous system, we performed paired recordings between mossy fiber terminals and CA3 pyramidal neurons in rat hippocampus. Millimolar concentrations of both the fast Ca^2+ chelator BAPTA [1,2-bis(2-aminophenoxy)ethane- N,N, N′,N′-tetraacetic acid] and the slow chelator EGTA efficiently suppressed transmitter release, indicating loose coupling between Ca^2+ channels and release sensors. Loose coupling enabled the control of initial release probability by fast endogenous Ca^2+ buffers and the generation of facilitation by buffer saturation. Thus, loose coupling provides the molecular framework for presynaptic plasticity. article_processing_charge: No author: - first_name: Nicholas full_name: Vyleta, Nicholas id: 36C4978E-F248-11E8-B48F-1D18A9856A87 last_name: Vyleta - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Vyleta N, Jonas PM. Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse. Science. 2014;343(6171):665-670. doi:10.1126/science.1244811 apa: Vyleta, N., & Jonas, P. M. (2014). Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.1244811 chicago: Vyleta, Nicholas, and Peter M Jonas. “Loose Coupling between Ca^2+ Channels and Release Sensors at a Plastic Hippocampal Synapse.” Science. American Association for the Advancement of Science, 2014. https://doi.org/10.1126/science.1244811. ieee: N. Vyleta and P. M. Jonas, “Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse,” Science, vol. 343, no. 6171. American Association for the Advancement of Science, pp. 665–670, 2014. ista: Vyleta N, Jonas PM. 2014. Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse. Science. 343(6171), 665–670. mla: Vyleta, Nicholas, and Peter M. Jonas. “Loose Coupling between Ca^2+ Channels and Release Sensors at a Plastic Hippocampal Synapse.” Science, vol. 343, no. 6171, American Association for the Advancement of Science, 2014, pp. 665–70, doi:10.1126/science.1244811. short: N. Vyleta, P.M. Jonas, Science 343 (2014) 665–670. corr_author: '1' date_created: 2018-12-11T11:56:27Z date_published: 2014-02-01T00:00:00Z date_updated: 2025-09-29T11:24:38Z day: '01' department: - _id: PeJo doi: 10.1126/science.1244811 ec_funded: 1 external_id: isi: - '000330724000044' intvolume: ' 343' isi: 1 issue: '6171' language: - iso: eng main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617475/ month: '02' oa: 1 oa_version: Submitted Version page: 665 - 670 project: - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons publication: Science publication_identifier: issn: - 0036-8075 publication_status: published publisher: American Association for the Advancement of Science publist_id: '4732' quality_controlled: '1' scopus_import: '1' status: public title: Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse type: journal_article user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345 volume: 343 year: '2014' ... --- _id: '2230' abstract: - lang: eng text: Intracellular electrophysiological recordings provide crucial insights into elementary neuronal signals such as action potentials and synaptic currents. Analyzing and interpreting these signals is essential for a quantitative understanding of neuronal information processing, and requires both fast data visualization and ready access to complex analysis routines. To achieve this goal, we have developed Stimfit, a free software package for cellular neurophysiology with a Python scripting interface and a built-in Python shell. The program supports most standard file formats for cellular neurophysiology and other biomedical signals through the Biosig library. To quantify and interpret the activity of single neurons and communication between neurons, the program includes algorithms to characterize the kinetics of presynaptic action potentials and postsynaptic currents, estimate latencies between pre- and postsynaptic events, and detect spontaneously occurring events. We validate and benchmark these algorithms, give estimation errors, and provide sample use cases, showing that Stimfit represents an efficient, accessible and extensible way to accurately analyze and interpret neuronal signals. article_number: '16' 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: Christoph full_name: Schmidt Hieber, Christoph last_name: Schmidt Hieber citation: ama: 'Guzmán J, Schlögl A, Schmidt Hieber C. Stimfit: Quantifying electrophysiological data with Python. Frontiers in Neuroinformatics. 2014;8(FEB). doi:10.3389/fninf.2014.00016' apa: 'Guzmán, J., Schlögl, A., & Schmidt Hieber, C. (2014). Stimfit: Quantifying electrophysiological data with Python. Frontiers in Neuroinformatics. Frontiers Research Foundation. https://doi.org/10.3389/fninf.2014.00016' chicago: 'Guzmán, José, Alois Schlögl, and Christoph Schmidt Hieber. “Stimfit: Quantifying Electrophysiological Data with Python.” Frontiers in Neuroinformatics. Frontiers Research Foundation, 2014. https://doi.org/10.3389/fninf.2014.00016.' ieee: 'J. Guzmán, A. Schlögl, and C. Schmidt Hieber, “Stimfit: Quantifying electrophysiological data with Python,” Frontiers in Neuroinformatics, vol. 8, no. FEB. Frontiers Research Foundation, 2014.' ista: 'Guzmán J, Schlögl A, Schmidt Hieber C. 2014. Stimfit: Quantifying electrophysiological data with Python. Frontiers in Neuroinformatics. 8(FEB), 16.' mla: 'Guzmán, José, et al. “Stimfit: Quantifying Electrophysiological Data with Python.” Frontiers in Neuroinformatics, vol. 8, no. FEB, 16, Frontiers Research Foundation, 2014, doi:10.3389/fninf.2014.00016.' short: J. Guzmán, A. Schlögl, C. Schmidt Hieber, Frontiers in Neuroinformatics 8 (2014). date_created: 2018-12-11T11:56:27Z date_published: 2014-02-21T00:00:00Z date_updated: 2025-09-29T11:24:02Z day: '21' ddc: - '570' department: - _id: ScienComp - _id: PeJo doi: 10.3389/fninf.2014.00016 external_id: isi: - '000348105900001' file: - access_level: open_access checksum: eeca00bba7232ff7d27db83321f6ea30 content_type: application/pdf creator: system date_created: 2018-12-12T10:12:17Z date_updated: 2020-07-14T12:45:34Z file_id: '4935' file_name: IST-2016-425-v1+1_fninf-08-00016.pdf file_size: 2883372 relation: main_file file_date_updated: 2020-07-14T12:45:34Z has_accepted_license: '1' intvolume: ' 8' isi: 1 issue: FEB language: - iso: eng month: '02' oa: 1 oa_version: Published Version publication: Frontiers in Neuroinformatics publication_identifier: issn: - 1662-5196 publication_status: published publisher: Frontiers Research Foundation publist_id: '4731' pubrep_id: '425' quality_controlled: '1' scopus_import: '1' status: public title: 'Stimfit: Quantifying electrophysiological data with Python' tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345 volume: 8 year: '2014' ... --- _id: '2254' abstract: - lang: eng text: Theta-gamma network oscillations are thought to represent key reference signals for information processing in neuronal ensembles, but the underlying synaptic mechanisms remain unclear. To address this question, we performed whole-cell (WC) patch-clamp recordings from mature hippocampal granule cells (GCs) in vivo in the dentate gyrus of anesthetized and awake rats. GCs in vivo fired action potentials at low frequency, consistent with sparse coding in the dentate gyrus. GCs were exposed to barrages of fast AMPAR-mediated excitatory postsynaptic currents (EPSCs), primarily relayed from the entorhinal cortex, and inhibitory postsynaptic currents (IPSCs), presumably generated by local interneurons. EPSCs exhibited coherence with the field potential predominantly in the theta frequency band, whereas IPSCs showed coherence primarily in the gamma range. Action potentials in GCs were phase locked to network oscillations. Thus, theta-gamma-modulated synaptic currents may provide a framework for sparse temporal coding of information in the dentate gyrus. article_processing_charge: No author: - first_name: Alejandro full_name: Pernia-Andrade, Alejandro id: 36963E98-F248-11E8-B48F-1D18A9856A87 last_name: Pernia-Andrade - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: ama: Pernia-Andrade A, Jonas PM. Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations. Neuron. 2014;81(1):140-152. doi:10.1016/j.neuron.2013.09.046 apa: Pernia-Andrade, A., & Jonas, P. M. (2014). Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2013.09.046 chicago: Pernia-Andrade, Alejandro, and Peter M Jonas. “Theta-Gamma-Modulated Synaptic Currents in Hippocampal Granule Cells in Vivo Define a Mechanism for Network Oscillations.” Neuron. Elsevier, 2014. https://doi.org/10.1016/j.neuron.2013.09.046. ieee: A. Pernia-Andrade and P. M. Jonas, “Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations,” Neuron, vol. 81, no. 1. Elsevier, pp. 140–152, 2014. ista: Pernia-Andrade A, Jonas PM. 2014. Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations. Neuron. 81(1), 140–152. mla: Pernia-Andrade, Alejandro, and Peter M. Jonas. “Theta-Gamma-Modulated Synaptic Currents in Hippocampal Granule Cells in Vivo Define a Mechanism for Network Oscillations.” Neuron, vol. 81, no. 1, Elsevier, 2014, pp. 140–52, doi:10.1016/j.neuron.2013.09.046. short: A. Pernia-Andrade, P.M. Jonas, Neuron 81 (2014) 140–152. corr_author: '1' date_created: 2018-12-11T11:56:35Z date_published: 2014-01-08T00:00:00Z date_updated: 2026-04-16T10:08:53Z day: '08' ddc: - '570' department: - _id: PeJo doi: 10.1016/j.neuron.2013.09.046 ec_funded: 1 external_id: isi: - '000329559000015' file: - access_level: open_access checksum: 438547cfcd9045a22f065f2019f07849 content_type: application/pdf creator: system date_created: 2018-12-12T10:09:48Z date_updated: 2020-07-14T12:45:35Z file_id: '4773' file_name: IST-2016-422-v1+1_1-s2.0-S0896627313009227-main.pdf file_size: 4373072 relation: main_file file_date_updated: 2020-07-14T12:45:35Z has_accepted_license: '1' intvolume: ' 81' isi: 1 issue: '1' language: - iso: eng month: '01' oa: 1 oa_version: Published Version page: 140 - 152 project: - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses publication: Neuron publication_identifier: issn: - 0896-6273 publication_status: published publisher: Elsevier publist_id: '4692' pubrep_id: '422' quality_controlled: '1' scopus_import: '1' status: public title: Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations type: journal_article user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd volume: 81 year: '2014' ... --- _id: '2285' abstract: - lang: eng text: GABAergic inhibitory interneurons control fundamental aspects of neuronal network function. Their functional roles are assumed to be defined by the identity of their input synapses, the architecture of their dendritic tree, the passive and active membrane properties and finally the nature of their postsynaptic targets. Indeed, interneurons display a high degree of morphological and physiological heterogeneity. However, whether their morphological and physiological characteristics are correlated and whether interneuron diversity can be described by a continuum of GABAergic cell types or by distinct classes has remained unclear. Here we perform a detailed morphological and physiological characterization of GABAergic cells in the dentate gyrus, the input region of the hippocampus. To achieve an unbiased and efficient sampling and classification we used knock-in mice expressing the enhanced green fluorescent protein (eGFP) in glutamate decarboxylase 67 (GAD67)-positive neurons and performed cluster analysis. We identified five interneuron classes, each of them characterized by a distinct set of anatomical and physiological parameters. Cross-correlation analysis further revealed a direct relation between morphological and physiological properties indicating that dentate gyrus interneurons fall into functionally distinct classes which may differentially control neuronal network activity. acknowledgement: 'Funded by Deutsche Forschungsgemeinschaft. Grant Numbers: SFB 505, SFB 780, BA1582/2-1 Excellence Initiative of the German Research Foundation (Spemann Graduate School). Grant Number: GSC-4 Lichtenberg Professorship-Award (VW-Foundation); Schram-Foundation; Excellence Initiative Brain Links-Brain Tools. The authors thank Drs. Jonas-Frederic Sauer and Claudio Elgueta for critically reading the manuscript. They also thank Karin Winterhalter, Margit Northemann and Ulrich Nöller for technical assistance.' article_processing_charge: No author: - first_name: Jonas full_name: Hosp, Jonas last_name: Hosp - first_name: Michael full_name: Strüber, Michael last_name: Strüber - first_name: Yuchio full_name: Yanagawa, Yuchio last_name: Yanagawa - first_name: Kunihiko full_name: Obata, Kunihiko last_name: Obata - first_name: Imre full_name: Vida, Imre last_name: Vida - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 - first_name: Marlene full_name: Bartos, Marlene last_name: Bartos citation: ama: Hosp J, Strüber M, Yanagawa Y, et al. Morpho-physiological criteria divide dentate gyrus interneurons into classes. Hippocampus. 2014;23(2):189-203. doi:10.1002/hipo.22214 apa: Hosp, J., Strüber, M., Yanagawa, Y., Obata, K., Vida, I., Jonas, P. M., & Bartos, M. (2014). Morpho-physiological criteria divide dentate gyrus interneurons into classes. Hippocampus. Wiley-Blackwell. https://doi.org/10.1002/hipo.22214 chicago: Hosp, Jonas, Michael Strüber, Yuchio Yanagawa, Kunihiko Obata, Imre Vida, Peter M Jonas, and Marlene Bartos. “Morpho-Physiological Criteria Divide Dentate Gyrus Interneurons into Classes.” Hippocampus. Wiley-Blackwell, 2014. https://doi.org/10.1002/hipo.22214. ieee: J. Hosp et al., “Morpho-physiological criteria divide dentate gyrus interneurons into classes,” Hippocampus, vol. 23, no. 2. Wiley-Blackwell, pp. 189–203, 2014. ista: Hosp J, Strüber M, Yanagawa Y, Obata K, Vida I, Jonas PM, Bartos M. 2014. Morpho-physiological criteria divide dentate gyrus interneurons into classes. Hippocampus. 23(2), 189–203. mla: Hosp, Jonas, et al. “Morpho-Physiological Criteria Divide Dentate Gyrus Interneurons into Classes.” Hippocampus, vol. 23, no. 2, Wiley-Blackwell, 2014, pp. 189–203, doi:10.1002/hipo.22214. short: J. Hosp, M. Strüber, Y. Yanagawa, K. Obata, I. Vida, P.M. Jonas, M. Bartos, Hippocampus 23 (2014) 189–203. date_created: 2018-12-11T11:56:46Z date_published: 2014-02-01T00:00:00Z date_updated: 2025-09-29T11:11:47Z day: '01' ddc: - '570' department: - _id: PeJo doi: 10.1002/hipo.22214 external_id: isi: - '000329879300006' file: - access_level: open_access checksum: ff6bc75a79dbc985a2e31b79253e6444 content_type: application/pdf creator: system date_created: 2018-12-12T10:15:54Z date_updated: 2020-07-14T12:45:37Z file_id: '5178' file_name: IST-2016-461-v1+1_Hosp_et_al-2014-Hippocampus.pdf file_size: 801589 relation: main_file file_date_updated: 2020-07-14T12:45:37Z has_accepted_license: '1' intvolume: ' 23' isi: 1 issue: '2' language: - iso: eng month: '02' oa: 1 oa_version: Published Version page: 189 - 203 publication: Hippocampus publication_status: published publisher: Wiley-Blackwell publist_id: '4646' pubrep_id: '461' quality_controlled: '1' scopus_import: '1' status: public title: Morpho-physiological criteria divide dentate gyrus interneurons into classes tmp: image: /images/cc_by_nc.png legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) short: CC BY-NC (4.0) type: journal_article user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345 volume: 23 year: '2014' ... --- _id: '2164' abstract: - lang: eng text: 'Neuronal ectopia, such as granule cell dispersion (GCD) in temporal lobe epilepsy (TLE), has been assumed to result from a migration defect during development. Indeed, recent studies reported that aberrant migration of neonatal-generated dentate granule cells (GCs) increased the risk to develop epilepsy later in life. On the contrary, in the present study, we show that fully differentiated GCs become motile following the induction of epileptiform activity, resulting in GCD. Hippocampal slice cultures from transgenic mice expressing green fluorescent protein in differentiated, but not in newly generated GCs, were incubated with the glutamate receptor agonist kainate (KA), which induced GC burst activity and GCD. Using real-time microscopy, we observed that KA-exposed, differentiated GCs translocated their cell bodies and changed their dendritic organization. As found in human TLE, KA application was associated with decreased expression of the extracellular matrix protein Reelin, particularly in hilar interneurons. Together these findings suggest that KA-induced motility of differentiated GCs contributes to the development of GCD and establish slice cultures as a model to study neuronal changes induced by epileptiform activity. ' article_processing_charge: No author: - first_name: Xuejun full_name: Chai, Xuejun last_name: Chai - first_name: Gert full_name: Münzner, Gert last_name: Münzner - first_name: Shanting full_name: Zhao, Shanting last_name: Zhao - first_name: Stefanie full_name: Tinnes, Stefanie last_name: Tinnes - first_name: Janina full_name: Kowalski, Janina id: 3F3CA136-F248-11E8-B48F-1D18A9856A87 last_name: Kowalski - first_name: Ute full_name: Häussler, Ute last_name: Häussler - first_name: Christina full_name: Young, Christina last_name: Young - first_name: Carola full_name: Haas, Carola last_name: Haas - first_name: Michael full_name: Frotscher, Michael last_name: Frotscher citation: ama: Chai X, Münzner G, Zhao S, et al. Epilepsy-induced motility of differentiated neurons. Cerebral Cortex. 2014;24(8):2130-2140. doi:10.1093/cercor/bht067 apa: Chai, X., Münzner, G., Zhao, S., Tinnes, S., Kowalski, J., Häussler, U., … Frotscher, M. (2014). Epilepsy-induced motility of differentiated neurons. Cerebral Cortex. Oxford University Press. https://doi.org/10.1093/cercor/bht067 chicago: Chai, Xuejun, Gert Münzner, Shanting Zhao, Stefanie Tinnes, Janina Kowalski, Ute Häussler, Christina Young, Carola Haas, and Michael Frotscher. “Epilepsy-Induced Motility of Differentiated Neurons.” Cerebral Cortex. Oxford University Press, 2014. https://doi.org/10.1093/cercor/bht067. ieee: X. Chai et al., “Epilepsy-induced motility of differentiated neurons,” Cerebral Cortex, vol. 24, no. 8. Oxford University Press, pp. 2130–2140, 2014. ista: Chai X, Münzner G, Zhao S, Tinnes S, Kowalski J, Häussler U, Young C, Haas C, Frotscher M. 2014. Epilepsy-induced motility of differentiated neurons. Cerebral Cortex. 24(8), 2130–2140. mla: Chai, Xuejun, et al. “Epilepsy-Induced Motility of Differentiated Neurons.” Cerebral Cortex, vol. 24, no. 8, Oxford University Press, 2014, pp. 2130–40, doi:10.1093/cercor/bht067. short: X. Chai, G. Münzner, S. Zhao, S. Tinnes, J. Kowalski, U. Häussler, C. Young, C. Haas, M. Frotscher, Cerebral Cortex 24 (2014) 2130–2140. date_created: 2018-12-11T11:56:04Z date_published: 2014-08-01T00:00:00Z date_updated: 2025-09-29T11:41:17Z day: '01' department: - _id: PeJo doi: 10.1093/cercor/bht067 external_id: isi: - '000340068500014' intvolume: ' 24' isi: 1 issue: '8' language: - iso: eng month: '08' oa_version: None page: 2130 - 2140 publication: Cerebral Cortex publication_status: published publisher: Oxford University Press publist_id: '4820' quality_controlled: '1' scopus_import: '1' status: public title: Epilepsy-induced motility of differentiated neurons type: journal_article user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345 volume: 24 year: '2014' ... --- _id: '2176' abstract: - lang: eng text: Electron microscopy (EM) allows for the simultaneous visualization of all tissue components at high resolution. However, the extent to which conventional aldehyde fixation and ethanol dehydration of the tissue alter the fine structure of cells and organelles, thereby preventing detection of subtle structural changes induced by an experiment, has remained an issue. Attempts have been made to rapidly freeze tissue to preserve native ultrastructure. Shock-freezing of living tissue under high pressure (high-pressure freezing, HPF) followed by cryosubstitution of the tissue water avoids aldehyde fixation and dehydration in ethanol; the tissue water is immobilized in â ̂1/450 ms, and a close-to-native fine structure of cells, organelles and molecules is preserved. Here we describe a protocol for HPF that is useful to monitor ultrastructural changes associated with functional changes at synapses in the brain but can be applied to many other tissues as well. The procedure requires a high-pressure freezer and takes a minimum of 7 d but can be paused at several points. article_processing_charge: No author: - first_name: Daniel full_name: Studer, Daniel last_name: Studer - first_name: Shanting full_name: Zhao, Shanting last_name: Zhao - first_name: Xuejun full_name: Chai, Xuejun last_name: Chai - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 - first_name: Werner full_name: Graber, Werner last_name: Graber - first_name: Sigrun full_name: Nestel, Sigrun last_name: Nestel - first_name: Michael full_name: Frotscher, Michael last_name: Frotscher citation: ama: Studer D, Zhao S, Chai X, et al. Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue. Nature Protocols. 2014;9(6):1480-1495. doi:10.1038/nprot.2014.099 apa: Studer, D., Zhao, S., Chai, X., Jonas, P. M., Graber, W., Nestel, S., & Frotscher, M. (2014). Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue. Nature Protocols. Nature Publishing Group. https://doi.org/10.1038/nprot.2014.099 chicago: Studer, Daniel, Shanting Zhao, Xuejun Chai, Peter M Jonas, Werner Graber, Sigrun Nestel, and Michael Frotscher. “Capture of Activity-Induced Ultrastructural Changes at Synapses by High-Pressure Freezing of Brain Tissue.” Nature Protocols. Nature Publishing Group, 2014. https://doi.org/10.1038/nprot.2014.099. ieee: D. Studer et al., “Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue,” Nature Protocols, vol. 9, no. 6. Nature Publishing Group, pp. 1480–1495, 2014. ista: Studer D, Zhao S, Chai X, Jonas PM, Graber W, Nestel S, Frotscher M. 2014. Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue. Nature Protocols. 9(6), 1480–1495. mla: Studer, Daniel, et al. “Capture of Activity-Induced Ultrastructural Changes at Synapses by High-Pressure Freezing of Brain Tissue.” Nature Protocols, vol. 9, no. 6, Nature Publishing Group, 2014, pp. 1480–95, doi:10.1038/nprot.2014.099. short: D. Studer, S. Zhao, X. Chai, P.M. Jonas, W. Graber, S. Nestel, M. Frotscher, Nature Protocols 9 (2014) 1480–1495. date_created: 2018-12-11T11:56:09Z date_published: 2014-05-29T00:00:00Z date_updated: 2025-09-29T11:36:43Z day: '29' department: - _id: PeJo doi: 10.1038/nprot.2014.099 external_id: isi: - '000337145800020' intvolume: ' 9' isi: 1 issue: '6' language: - iso: eng month: '05' oa_version: None page: 1480 - 1495 project: - _id: 25BDE9A4-B435-11E9-9278-68D0E5697425 grant_number: SFB-TR3-TP10B name: "Glutamaterge synaptische Ã\x9Cbertragung und Plastizität in hippocampalen Mikroschaltkreisen" publication: Nature Protocols publication_status: published publisher: Nature Publishing Group publist_id: '4807' quality_controlled: '1' scopus_import: '1' status: public title: Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue type: journal_article user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345 volume: 9 year: '2014' ...