[{"file_date_updated":"2020-07-14T12:44:44Z","year":"2016","publist_id":"5947","date_published":"2016-10-25T00:00:00Z","_id":"1323","external_id":{"isi":["000387034600001"]},"acknowledged_ssus":[{"_id":"M-Shop"},{"_id":"PreCl"}],"date_created":"2018-12-11T11:51:22Z","publication":"eLife","type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","article_processing_charge":"No","day":"25","file":[{"relation":"main_file","date_created":"2018-12-12T10:17:05Z","file_size":1477891,"creator":"system","access_level":"open_access","file_name":"IST-2016-715-v1+1_e17977-download.pdf","date_updated":"2020-07-14T12:44:44Z","content_type":"application/pdf","checksum":"a7201280c571bed88ebd459ce5ce6a47","file_id":"5257"}],"publisher":"eLife Sciences Publications","abstract":[{"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.","lang":"eng"}],"quality_controlled":"1","title":"Plasticity-dependent, full detonation at hippocampal mossy fiber–CA3 pyramidal neuron synapses","oa":1,"tmp":{"image":"/images/cc_by.png","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"project":[{"_id":"25C0F108-B435-11E9-9278-68D0E5697425","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","grant_number":"268548","call_identifier":"FP7"},{"call_identifier":"H2020","_id":"25B7EB9E-B435-11E9-9278-68D0E5697425","grant_number":"692692","name":"Biophysics and circuit function of a giant cortical glutamatergic synapse"}],"date_updated":"2025-09-22T08:26:29Z","doi":"10.7554/eLife.17977","status":"public","oa_version":"Published Version","language":[{"iso":"eng"}],"pubrep_id":"715","month":"10","volume":5,"publication_status":"published","isi":1,"author":[{"full_name":"Vyleta, Nicholas","last_name":"Vyleta","first_name":"Nicholas","id":"36C4978E-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Borges Merjane","full_name":"Borges Merjane, Carolina","orcid":"0000-0003-0005-401X","first_name":"Carolina","id":"4305C450-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Jonas","full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804","first_name":"Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"}],"department":[{"_id":"PeJo"}],"ddc":["571","572"],"intvolume":"         5","scopus_import":"1","article_number":"e17977","corr_author":"1","citation":{"apa":"Vyleta, N., Borges Merjane, C., &#38; Jonas, P. M. (2016). Plasticity-dependent, full detonation at hippocampal mossy fiber–CA3 pyramidal neuron synapses. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/eLife.17977\">https://doi.org/10.7554/eLife.17977</a>","ama":"Vyleta N, Borges Merjane C, Jonas PM. Plasticity-dependent, full detonation at hippocampal mossy fiber–CA3 pyramidal neuron synapses. <i>eLife</i>. 2016;5. doi:<a href=\"https://doi.org/10.7554/eLife.17977\">10.7554/eLife.17977</a>","short":"N. Vyleta, C. Borges Merjane, P.M. Jonas, ELife 5 (2016).","mla":"Vyleta, Nicholas, et al. “Plasticity-Dependent, Full Detonation at Hippocampal Mossy Fiber–CA3 Pyramidal Neuron Synapses.” <i>ELife</i>, vol. 5, e17977, eLife Sciences Publications, 2016, doi:<a href=\"https://doi.org/10.7554/eLife.17977\">10.7554/eLife.17977</a>.","ieee":"N. Vyleta, C. Borges Merjane, and P. M. Jonas, “Plasticity-dependent, full detonation at hippocampal mossy fiber–CA3 pyramidal neuron synapses,” <i>eLife</i>, vol. 5. eLife Sciences Publications, 2016.","chicago":"Vyleta, Nicholas, Carolina Borges Merjane, and Peter M Jonas. “Plasticity-Dependent, Full Detonation at Hippocampal Mossy Fiber–CA3 Pyramidal Neuron Synapses.” <i>ELife</i>. eLife Sciences Publications, 2016. <a href=\"https://doi.org/10.7554/eLife.17977\">https://doi.org/10.7554/eLife.17977</a>.","ista":"Vyleta N, Borges Merjane C, Jonas PM. 2016. Plasticity-dependent, full detonation at hippocampal mossy fiber–CA3 pyramidal neuron synapses. eLife. 5, e17977."},"ec_funded":1,"has_accepted_license":"1"},{"corr_author":"1","citation":{"ama":"Guzmán J, Schlögl A, Frotscher M, Jonas PM. Synaptic mechanisms of pattern completion in the hippocampal CA3 network. <i>Science</i>. 2016;353(6304):1117-1123. doi:<a href=\"https://doi.org/10.1126/science.aaf1836\">10.1126/science.aaf1836</a>","apa":"Guzmán, J., Schlögl, A., Frotscher, M., &#38; Jonas, P. M. (2016). Synaptic mechanisms of pattern completion in the hippocampal CA3 network. <i>Science</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/science.aaf1836\">https://doi.org/10.1126/science.aaf1836</a>","short":"J. Guzmán, A. Schlögl, M. Frotscher, P.M. Jonas, Science 353 (2016) 1117–1123.","ieee":"J. Guzmán, A. Schlögl, M. Frotscher, and P. M. Jonas, “Synaptic mechanisms of pattern completion in the hippocampal CA3 network,” <i>Science</i>, vol. 353, no. 6304. American Association for the Advancement of Science, pp. 1117–1123, 2016.","chicago":"Guzmán, José, Alois Schlögl, Michael Frotscher, and Peter M Jonas. “Synaptic Mechanisms of Pattern Completion in the Hippocampal CA3 Network.” <i>Science</i>. American Association for the Advancement of Science, 2016. <a href=\"https://doi.org/10.1126/science.aaf1836\">https://doi.org/10.1126/science.aaf1836</a>.","mla":"Guzmán, José, et al. “Synaptic Mechanisms of Pattern Completion in the Hippocampal CA3 Network.” <i>Science</i>, vol. 353, no. 6304, American Association for the Advancement of Science, 2016, pp. 1117–23, doi:<a href=\"https://doi.org/10.1126/science.aaf1836\">10.1126/science.aaf1836</a>.","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."},"issue":"6304","has_accepted_license":"1","ec_funded":1,"isi":1,"publication_status":"published","author":[{"last_name":"Guzmán","full_name":"Guzmán, José","orcid":"0000-0003-2209-5242","id":"30CC5506-F248-11E8-B48F-1D18A9856A87","first_name":"José"},{"id":"45BF87EE-F248-11E8-B48F-1D18A9856A87","first_name":"Alois","orcid":"0000-0002-5621-8100","last_name":"Schlögl","full_name":"Schlögl, Alois"},{"first_name":"Michael","last_name":"Frotscher","full_name":"Frotscher, Michael"},{"first_name":"Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","last_name":"Jonas","full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804"}],"department":[{"_id":"ScienComp"},{"_id":"PeJo"}],"month":"09","volume":353,"intvolume":"       353","ddc":["570"],"scopus_import":"1","language":[{"iso":"eng"}],"page":"1117 - 1123","oa_version":"Preprint","pubrep_id":"823","oa":1,"project":[{"grant_number":"268548","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","_id":"25C0F108-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"},{"call_identifier":"FWF","grant_number":"P24909-B24","name":"Mechanisms of transmitter release at GABAergic synapses","_id":"25C26B1E-B435-11E9-9278-68D0E5697425"}],"doi":"10.1126/science.aaf1836","date_updated":"2025-09-22T08:12:10Z","status":"public","publisher":"American Association for the Advancement of Science","quality_controlled":"1","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."}],"title":"Synaptic mechanisms of pattern completion in the hippocampal CA3 network","file":[{"checksum":"89caefa4e181424cbf0aecc835fcc5ec","content_type":"application/pdf","file_id":"4945","date_updated":"2020-07-14T12:44:46Z","file_name":"IST-2017-823-v1+1_aaf1836_CombinedPDF_v2-1.pdf","file_size":19408143,"access_level":"open_access","creator":"system","relation":"main_file","date_created":"2018-12-12T10:12:27Z"}],"type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","publication":"Science","article_processing_charge":"No","day":"09","year":"2016","publist_id":"5899","file_date_updated":"2020-07-14T12:44:46Z","date_created":"2018-12-11T11:51:31Z","date_published":"2016-09-09T00:00:00Z","external_id":{"isi":["000382626800045"]},"_id":"1350","acknowledged_ssus":[{"_id":"ScienComp"}]},{"day":"01","article_processing_charge":"No","type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","publication":"Neural Plasticity","date_created":"2018-12-11T11:52:00Z","_id":"1435","external_id":{"isi":["000374056200001"]},"date_published":"2016-01-01T00:00:00Z","publist_id":"5762","year":"2016","file_date_updated":"2020-07-14T12:44:54Z","date_updated":"2025-09-18T11:45:18Z","doi":"10.1155/2016/1207393","status":"public","tmp":{"image":"/images/cc_by.png","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"oa":1,"quality_controlled":"1","abstract":[{"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.","lang":"eng"}],"title":"P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction","publisher":"Hindawi Publishing Corporation","file":[{"date_updated":"2020-07-14T12:44:54Z","checksum":"8dc5c2f3d44d4775a6e7e3edb0d7a0da","content_type":"application/pdf","file_id":"4740","access_level":"open_access","file_size":1395180,"creator":"system","date_created":"2018-12-12T10:09:17Z","relation":"main_file","file_name":"IST-2016-580-v1+1_1207393.pdf"}],"scopus_import":"1","ddc":["570"],"intvolume":"      2016","author":[{"orcid":"0000-0003-2209-5242","full_name":"Guzmán, José","last_name":"Guzmán","first_name":"José","id":"30CC5506-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Gerevich","full_name":"Gerevich, Zoltan","first_name":"Zoltan"}],"department":[{"_id":"PeJo"}],"publication_status":"published","isi":1,"month":"01","volume":2016,"pubrep_id":"580","language":[{"iso":"eng"}],"oa_version":"Published Version","has_accepted_license":"1","citation":{"apa":"Guzmán, J., &#38; Gerevich, Z. (2016). P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction. <i>Neural Plasticity</i>. Hindawi Publishing Corporation. <a href=\"https://doi.org/10.1155/2016/1207393\">https://doi.org/10.1155/2016/1207393</a>","ama":"Guzmán J, Gerevich Z. P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction. <i>Neural Plasticity</i>. 2016;2016. doi:<a href=\"https://doi.org/10.1155/2016/1207393\">10.1155/2016/1207393</a>","short":"J. Guzmán, Z. Gerevich, Neural Plasticity 2016 (2016).","mla":"Guzmán, José, and Zoltan Gerevich. “P2Y Receptors in Synaptic Transmission and Plasticity: Therapeutic Potential in Cognitive Dysfunction.” <i>Neural Plasticity</i>, vol. 2016, 1207393, Hindawi Publishing Corporation, 2016, doi:<a href=\"https://doi.org/10.1155/2016/1207393\">10.1155/2016/1207393</a>.","ieee":"J. Guzmán and Z. Gerevich, “P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction,” <i>Neural Plasticity</i>, vol. 2016. Hindawi Publishing Corporation, 2016.","chicago":"Guzmán, José, and Zoltan Gerevich. “P2Y Receptors in Synaptic Transmission and Plasticity: Therapeutic Potential in Cognitive Dysfunction.” <i>Neural Plasticity</i>. Hindawi Publishing Corporation, 2016. <a href=\"https://doi.org/10.1155/2016/1207393\">https://doi.org/10.1155/2016/1207393</a>.","ista":"Guzmán J, Gerevich Z. 2016. P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction. Neural Plasticity. 2016, 1207393."},"article_number":"1207393"},{"article_processing_charge":"No","day":"01","type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","publication":"Hippocampus","date_created":"2018-12-11T11:53:03Z","date_published":"2016-05-01T00:00:00Z","external_id":{"isi":["000374666700011"]},"_id":"1616","year":"2016","publist_id":"5550","file_date_updated":"2020-07-14T12:45:07Z","date_updated":"2025-09-18T10:58:31Z","doi":"10.1002/hipo.22550","status":"public","tmp":{"short":"CC BY-NC-ND (4.0)","image":"/images/cc_by_nc_nd.png","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode"},"oa":1,"publisher":"Wiley","title":"Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats","quality_controlled":"1","abstract":[{"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.","lang":"eng"}],"file":[{"date_created":"2018-12-12T10:13:47Z","relation":"main_file","file_size":905348,"creator":"system","access_level":"open_access","file_name":"IST-2016-469-v1+1_Kowalski_et_al-Hippocampus.pdf","date_updated":"2020-07-14T12:45:07Z","checksum":"284b72b12fbe15474833ed3d4549f86b","file_id":"5033","content_type":"application/pdf"}],"publication_identifier":{"issn":["1050-9631"],"eissn":["1098-1063"]},"ddc":["570"],"intvolume":"        26","scopus_import":"1","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.","publication_status":"published","isi":1,"department":[{"_id":"PeJo"}],"author":[{"last_name":"Kowalski","full_name":"Kowalski, Janina","first_name":"Janina","id":"3F3CA136-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Gan","full_name":"Gan, Jian","first_name":"Jian","id":"3614E438-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0001-5001-4804","last_name":"Jonas","full_name":"Jonas, Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","first_name":"Peter M"},{"id":"36963E98-F248-11E8-B48F-1D18A9856A87","first_name":"Alejandro","full_name":"Pernia-Andrade, Alejandro","last_name":"Pernia-Andrade"}],"month":"05","volume":26,"pubrep_id":"469","language":[{"iso":"eng"}],"page":"668 - 682","oa_version":"Published Version","has_accepted_license":"1","corr_author":"1","citation":{"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.","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.” <i>Hippocampus</i>. Wiley, 2016. <a href=\"https://doi.org/10.1002/hipo.22550\">https://doi.org/10.1002/hipo.22550</a>.","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,” <i>Hippocampus</i>, vol. 26, no. 5. Wiley, pp. 668–682, 2016.","mla":"Kowalski, Janina, et al. “Intrinsic Membrane Properties Determine Hippocampal Differential Firing Pattern in Vivo in Anesthetized Rats.” <i>Hippocampus</i>, vol. 26, no. 5, Wiley, 2016, pp. 668–82, doi:<a href=\"https://doi.org/10.1002/hipo.22550\">10.1002/hipo.22550</a>.","short":"J. Kowalski, J. Gan, P.M. Jonas, A. Pernia-Andrade, Hippocampus 26 (2016) 668–682.","ama":"Kowalski J, Gan J, Jonas PM, Pernia-Andrade A. Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats. <i>Hippocampus</i>. 2016;26(5):668-682. doi:<a href=\"https://doi.org/10.1002/hipo.22550\">10.1002/hipo.22550</a>","apa":"Kowalski, J., Gan, J., Jonas, P. M., &#38; Pernia-Andrade, A. (2016). Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats. <i>Hippocampus</i>. Wiley. <a href=\"https://doi.org/10.1002/hipo.22550\">https://doi.org/10.1002/hipo.22550</a>"},"issue":"5"},{"scopus_import":"1","intvolume":"         7","ddc":["570"],"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. ","department":[{"_id":"PeJo"}],"author":[{"first_name":"Rajiv Kumar","id":"46CB58F2-F248-11E8-B48F-1D18A9856A87","full_name":"Mishra, Rajiv Kumar","last_name":"Mishra"},{"full_name":"Kim, Sooyun","last_name":"Kim","id":"394AB1C8-F248-11E8-B48F-1D18A9856A87","first_name":"Sooyun"},{"first_name":"José","id":"30CC5506-F248-11E8-B48F-1D18A9856A87","last_name":"Guzmán","full_name":"Guzmán, José","orcid":"0000-0003-2209-5242"},{"id":"353C1B58-F248-11E8-B48F-1D18A9856A87","first_name":"Peter M","orcid":"0000-0001-5001-4804","last_name":"Jonas","full_name":"Jonas, Peter M"}],"isi":1,"publication_status":"published","volume":7,"month":"05","pubrep_id":"582","language":[{"iso":"eng"}],"oa_version":"Published Version","has_accepted_license":"1","related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"1396"}]},"ec_funded":1,"citation":{"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.","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,” <i>Nature Communications</i>, vol. 7. Nature Publishing Group, 2016.","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.” <i>Nature Communications</i>. Nature Publishing Group, 2016. <a href=\"https://doi.org/10.1038/ncomms11552\">https://doi.org/10.1038/ncomms11552</a>.","mla":"Mishra, Rajiv Kumar, et al. “Symmetric Spike Timing-Dependent Plasticity at CA3–CA3 Synapses Optimizes Storage and Recall in Autoassociative Networks.” <i>Nature Communications</i>, vol. 7, 11552, Nature Publishing Group, 2016, doi:<a href=\"https://doi.org/10.1038/ncomms11552\">10.1038/ncomms11552</a>.","short":"R.K. Mishra, S. Kim, J. Guzmán, P.M. Jonas, Nature Communications 7 (2016).","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. <i>Nature Communications</i>. 2016;7. doi:<a href=\"https://doi.org/10.1038/ncomms11552\">10.1038/ncomms11552</a>","apa":"Mishra, R. K., Kim, S., Guzmán, J., &#38; Jonas, P. M. (2016). Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative networks. <i>Nature Communications</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/ncomms11552\">https://doi.org/10.1038/ncomms11552</a>"},"corr_author":"1","article_number":"11552","day":"13","article_processing_charge":"No","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","type":"journal_article","publication":"Nature Communications","date_created":"2018-12-11T11:51:59Z","_id":"1432","external_id":{"isi":["000375938200001"]},"date_published":"2016-05-13T00:00:00Z","publist_id":"5766","year":"2016","file_date_updated":"2020-07-14T12:44:53Z","date_updated":"2026-07-29T11:31:52Z","status":"public","doi":"10.1038/ncomms11552","project":[{"_id":"25C26B1E-B435-11E9-9278-68D0E5697425","name":"Mechanisms of transmitter release at GABAergic synapses","grant_number":"P24909-B24","call_identifier":"FWF"},{"call_identifier":"FP7","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","grant_number":"268548","_id":"25C0F108-B435-11E9-9278-68D0E5697425"}],"tmp":{"image":"/images/cc_by.png","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"oa":1,"title":"Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative networks","quality_controlled":"1","abstract":[{"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.","lang":"eng"}],"publisher":"Nature Publishing Group","file":[{"relation":"main_file","date_created":"2018-12-12T10:18:33Z","file_size":4510512,"access_level":"open_access","creator":"system","file_name":"IST-2016-582-v1+1_ncomms11552.pdf","date_updated":"2020-07-14T12:44:53Z","checksum":"7e84d0392348c874d473b62f1042de22","content_type":"application/pdf","file_id":"5355"}]},{"page":"83","oa_version":"Published Version","language":[{"iso":"eng"}],"month":"03","publication_status":"published","author":[{"last_name":"Mishra","full_name":"Mishra, Rajiv Kumar","first_name":"Rajiv Kumar","id":"46CB58F2-F248-11E8-B48F-1D18A9856A87"}],"department":[{"_id":"PeJo"},{"_id":"GradSch"}],"ddc":["570"],"corr_author":"1","citation":{"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.","mla":"Mishra, Rajiv Kumar. <i>Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses in Hippocampus</i>. 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.","ama":"Mishra RK. Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus. 2016.","apa":"Mishra, R. K. (2016). <i>Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus</i>. Institute of Science and Technology Austria.","short":"R.K. Mishra, Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses in Hippocampus, Institute of Science and Technology Austria, 2016."},"alternative_title":["ISTA Thesis"],"related_material":{"record":[{"relation":"part_of_dissertation","status":"public","id":"1432"}]},"degree_awarded":"PhD","has_accepted_license":"1","OA_place":"publisher","supervisor":[{"last_name":"Jonas","full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804","first_name":"Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"}],"file_date_updated":"2021-02-22T11:48:44Z","doi_confirm":"1","year":"2016","publist_id":"5811","date_published":"2016-03-01T00:00:00Z","_id":"1396","date_created":"2018-12-11T11:51:46Z","type":"dissertation","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","article_processing_charge":"No","day":"01","publication_identifier":{"issn":["2663-337X"]},"file":[{"checksum":"5a010a838faf040f7064f3cfb802f743","content_type":"application/pdf","file_id":"6782","date_updated":"2020-07-14T12:44:48Z","file_name":"Thesis_Mishra_Rajiv (Final).pdf","creator":"dernst","file_size":2407572,"access_level":"closed","relation":"main_file","date_created":"2019-08-09T12:14:46Z"},{"checksum":"81b26d9ede92c99f1d8cc6fa1d04cbbb","file_id":"9183","content_type":"application/pdf","success":1,"date_updated":"2021-02-22T11:48:44Z","file_name":"2016_RajivMishra_Thesis.pdf","creator":"dernst","file_size":2407572,"access_level":"open_access","date_created":"2021-02-22T11:48:44Z","relation":"main_file"}],"publisher":"Institute of Science and Technology Austria","title":"Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus","abstract":[{"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.","lang":"eng"}],"oa":1,"status":"public","date_updated":"2026-07-29T11:31:52Z"},{"isi":1,"publication_status":"published","department":[{"_id":"PeJo"}],"author":[{"id":"3AE48E0A-F248-11E8-B48F-1D18A9856A87","first_name":"David H","orcid":"0000-0001-7577-1676","full_name":"Vandael, David H","last_name":"Vandael"},{"full_name":"Marcantoni, Andrea","last_name":"Marcantoni","first_name":"Andrea"},{"full_name":"Carbone, Emilio","last_name":"Carbone","first_name":"Emilio"}],"volume":8,"month":"10","intvolume":"         8","scopus_import":"1","acknowledgement":"This work was supported by the Italian MIUR (PRIN 2010/2011 project 2010JFYFY2) and the University of Torino.","language":[{"iso":"eng"}],"page":"149 - 161","oa_version":"Submitted Version","citation":{"mla":"Vandael, David H., et al. “Cav1.3 Channels as Key Regulators of Neuron-like Firings and Catecholamine Release in Chromaffin Cells.” <i>Current Molecular Pharmacology</i>, vol. 8, no. 2, Bentham Science Publishers, 2015, pp. 149–61, doi:<a href=\"https://doi.org/10.2174/1874467208666150507105443\">10.2174/1874467208666150507105443</a>.","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,” <i>Current Molecular Pharmacology</i>, vol. 8, no. 2. Bentham Science Publishers, pp. 149–161, 2015.","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.” <i>Current Molecular Pharmacology</i>. Bentham Science Publishers, 2015. <a href=\"https://doi.org/10.2174/1874467208666150507105443\">https://doi.org/10.2174/1874467208666150507105443</a>.","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.","apa":"Vandael, D. H., Marcantoni, A., &#38; Carbone, E. (2015). Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells. <i>Current Molecular Pharmacology</i>. Bentham Science Publishers. <a href=\"https://doi.org/10.2174/1874467208666150507105443\">https://doi.org/10.2174/1874467208666150507105443</a>","ama":"Vandael DH, Marcantoni A, Carbone E. Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells. <i>Current Molecular Pharmacology</i>. 2015;8(2):149-161. doi:<a href=\"https://doi.org/10.2174/1874467208666150507105443\">10.2174/1874467208666150507105443</a>","short":"D.H. Vandael, A. Marcantoni, E. Carbone, Current Molecular Pharmacology 8 (2015) 149–161."},"issue":"2","type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","publication":"Current Molecular Pharmacology","article_processing_charge":"No","day":"01","year":"2015","publist_id":"5636","date_created":"2018-12-11T11:52:35Z","pmid":1,"date_published":"2015-10-01T00:00:00Z","_id":"1535","external_id":{"pmid":["25966692"],"isi":["000217186100005"]},"article_type":"original","oa":1,"doi":"10.2174/1874467208666150507105443","date_updated":"2025-09-23T08:12:18Z","status":"public","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384372/"}],"publisher":"Bentham Science Publishers","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."}],"quality_controlled":"1","title":"Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells"},{"page":"4835 - 4853","oa_version":"Submitted Version","language":[{"iso":"eng"}],"volume":593,"month":"11","isi":1,"publication_status":"published","author":[{"first_name":"Daniela","full_name":"Gavello, Daniela","last_name":"Gavello"},{"first_name":"David H","id":"3AE48E0A-F248-11E8-B48F-1D18A9856A87","last_name":"Vandael","full_name":"Vandael, David H","orcid":"0000-0001-7577-1676"},{"first_name":"Sara","full_name":"Gosso, Sara","last_name":"Gosso"},{"last_name":"Carbone","full_name":"Carbone, Emilio","first_name":"Emilio"},{"first_name":"Valentina","full_name":"Carabelli, Valentina","last_name":"Carabelli"}],"department":[{"_id":"PeJo"}],"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.","intvolume":"       593","scopus_import":"1","issue":"22","citation":{"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.” <i>Journal of Physiology</i>, vol. 593, no. 22, Wiley-Blackwell, 2015, pp. 4835–53, doi:<a href=\"https://doi.org/10.1113/JP271078\">10.1113/JP271078</a>.","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,” <i>Journal of Physiology</i>, vol. 593, no. 22. Wiley-Blackwell, pp. 4835–4853, 2015.","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.” <i>Journal of Physiology</i>. Wiley-Blackwell, 2015. <a href=\"https://doi.org/10.1113/JP271078\">https://doi.org/10.1113/JP271078</a>.","short":"D. Gavello, D.H. Vandael, S. Gosso, E. Carbone, V. Carabelli, Journal of Physiology 593 (2015) 4835–4853.","apa":"Gavello, D., Vandael, D. H., Gosso, S., Carbone, E., &#38; 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. <i>Journal of Physiology</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1113/JP271078\">https://doi.org/10.1113/JP271078</a>","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. <i>Journal of Physiology</i>. 2015;593(22):4835-4853. doi:<a href=\"https://doi.org/10.1113/JP271078\">10.1113/JP271078</a>"},"year":"2015","publist_id":"5606","date_published":"2015-11-15T00:00:00Z","external_id":{"pmid":["26282459"],"isi":["000365267700003"]},"_id":"1565","date_created":"2018-12-11T11:52:45Z","pmid":1,"publication":"Journal of Physiology","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","type":"journal_article","article_processing_charge":"No","day":"15","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4650409/"}],"publisher":"Wiley-Blackwell","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","abstract":[{"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.","lang":"eng"}],"quality_controlled":"1","oa":1,"status":"public","doi":"10.1113/JP271078","date_updated":"2025-09-23T08:30:00Z"},{"year":"2015","publist_id":"5591","file_date_updated":"2020-07-14T12:45:02Z","date_created":"2018-12-11T11:52:50Z","date_published":"2015-12-17T00:00:00Z","_id":"1580","external_id":{"isi":["000366144000037"]},"type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","publication":"Neuroscience","article_processing_charge":"No","day":"17","publisher":"Elsevier","title":"Knock-down of synapsin alters cell excitability and action potential waveform by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons","quality_controlled":"1","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."}],"file":[{"file_name":"2015_Neuroscience_Brenes.pdf","date_created":"2020-05-15T06:50:20Z","relation":"main_file","file_size":5563015,"creator":"dernst","access_level":"open_access","checksum":"af2c4c994718c7be417eba0dc746aac9","file_id":"7849","content_type":"application/pdf","date_updated":"2020-07-14T12:45:02Z"}],"tmp":{"short":"CC BY-NC-ND (4.0)","image":"/images/cc_by_nc_nd.png","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode"},"article_type":"original","oa":1,"date_updated":"2025-09-23T09:25:46Z","status":"public","doi":"10.1016/j.neuroscience.2015.10.046","language":[{"iso":"eng"}],"page":"430 - 443","oa_version":"Submitted Version","publication_status":"published","isi":1,"department":[{"_id":"PeJo"}],"author":[{"full_name":"Brenes, Oscar","last_name":"Brenes","first_name":"Oscar"},{"first_name":"David H","id":"3AE48E0A-F248-11E8-B48F-1D18A9856A87","last_name":"Vandael","full_name":"Vandael, David H","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"},{"full_name":"Ghirardi, Mirella","last_name":"Ghirardi","first_name":"Mirella"}],"month":"12","volume":311,"intvolume":"       311","ddc":["570"],"scopus_import":"1","citation":{"apa":"Brenes, O., Vandael, D. H., Carbone, E., Montarolo, P., &#38; 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. <i>Neuroscience</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuroscience.2015.10.046\">https://doi.org/10.1016/j.neuroscience.2015.10.046</a>","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. <i>Neuroscience</i>. 2015;311:430-443. doi:<a href=\"https://doi.org/10.1016/j.neuroscience.2015.10.046\">10.1016/j.neuroscience.2015.10.046</a>","short":"O. Brenes, D.H. Vandael, E. Carbone, P. Montarolo, M. Ghirardi, Neuroscience 311 (2015) 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.” <i>Neuroscience</i>, vol. 311, Elsevier, 2015, pp. 430–43, doi:<a href=\"https://doi.org/10.1016/j.neuroscience.2015.10.046\">10.1016/j.neuroscience.2015.10.046</a>.","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.” <i>Neuroscience</i>. Elsevier, 2015. <a href=\"https://doi.org/10.1016/j.neuroscience.2015.10.046\">https://doi.org/10.1016/j.neuroscience.2015.10.046</a>.","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,” <i>Neuroscience</i>, 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."},"has_accepted_license":"1"},{"oa":1,"date_updated":"2025-09-23T10:49:39Z","status":"public","doi":"10.1073/pnas.1412996112","project":[{"call_identifier":"FWF","_id":"25C26B1E-B435-11E9-9278-68D0E5697425","name":"Mechanisms of transmitter release at GABAergic synapses","grant_number":"P24909-B24"},{"call_identifier":"FP7","grant_number":"268548","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","_id":"25C0F108-B435-11E9-9278-68D0E5697425"}],"title":"Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells","quality_controlled":"1","abstract":[{"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. ","lang":"eng"}],"publisher":"National Academy of Sciences","file":[{"date_updated":"2020-07-14T12:45:07Z","content_type":"application/pdf","checksum":"6703309a1f58493cf5a704211fb6ebed","file_id":"5838","relation":"main_file","date_created":"2019-01-17T07:52:40Z","creator":"dernst","access_level":"open_access","file_size":1280860,"file_name":"2015_PNAS_Strueber.pdf"}],"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","type":"journal_article","publication":"PNAS","day":"27","article_processing_charge":"No","publist_id":"5552","year":"2015","file_date_updated":"2020-07-14T12:45:07Z","pmid":1,"date_created":"2018-12-11T11:53:02Z","_id":"1614","external_id":{"pmid":["25583495"],"isi":["000348417000066"]},"date_published":"2015-01-27T00:00:00Z","citation":{"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.","ieee":"M. Strüber, P. M. Jonas, and M. Bartos, “Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells,” <i>PNAS</i>, vol. 112, no. 4. National Academy of Sciences, pp. 1220–1225, 2015.","chicago":"Strüber, Michael, Peter M Jonas, and Marlene Bartos. “Strength and Duration of Perisomatic GABAergic Inhibition Depend on Distance between Synaptically Connected Cells.” <i>PNAS</i>. National Academy of Sciences, 2015. <a href=\"https://doi.org/10.1073/pnas.1412996112\">https://doi.org/10.1073/pnas.1412996112</a>.","mla":"Strüber, Michael, et al. “Strength and Duration of Perisomatic GABAergic Inhibition Depend on Distance between Synaptically Connected Cells.” <i>PNAS</i>, vol. 112, no. 4, National Academy of Sciences, 2015, pp. 1220–25, doi:<a href=\"https://doi.org/10.1073/pnas.1412996112\">10.1073/pnas.1412996112</a>.","short":"M. Strüber, P.M. Jonas, M. Bartos, PNAS 112 (2015) 1220–1225.","ama":"Strüber M, Jonas PM, Bartos M. Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells. <i>PNAS</i>. 2015;112(4):1220-1225. doi:<a href=\"https://doi.org/10.1073/pnas.1412996112\">10.1073/pnas.1412996112</a>","apa":"Strüber, M., Jonas, P. M., &#38; Bartos, M. (2015). Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells. <i>PNAS</i>. National Academy of Sciences. <a href=\"https://doi.org/10.1073/pnas.1412996112\">https://doi.org/10.1073/pnas.1412996112</a>"},"issue":"4","has_accepted_license":"1","ec_funded":1,"department":[{"_id":"PeJo"}],"author":[{"full_name":"Strüber, Michael","last_name":"Strüber","first_name":"Michael"},{"first_name":"Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804","last_name":"Jonas","full_name":"Jonas, Peter M"},{"full_name":"Bartos, Marlene","last_name":"Bartos","first_name":"Marlene"}],"publication_status":"published","isi":1,"volume":112,"month":"01","scopus_import":"1","intvolume":"       112","ddc":["570"],"language":[{"iso":"eng"}],"oa_version":"Published Version","page":"1220 - 1225"},{"tmp":{"image":"/images/cc_by.png","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"oa":1,"date_updated":"2025-09-23T09:48:31Z","status":"public","doi":"10.1016/j.celrep.2015.09.011","publisher":"Cell Press","abstract":[{"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.","lang":"eng"}],"title":"Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism","quality_controlled":"1","file":[{"access_level":"open_access","creator":"system","file_size":2314406,"date_created":"2018-12-12T10:13:23Z","relation":"main_file","file_name":"IST-2016-470-v1+1_1-s2.0-S2211124715010220-main.pdf","date_updated":"2020-07-14T12:45:07Z","file_id":"5005","checksum":"44d30fbb543774b076b4938bd36af9d7","content_type":"application/pdf"}],"type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","publication":"Cell Reports","article_processing_charge":"No","day":"20","year":"2015","publist_id":"5551","file_date_updated":"2020-07-14T12:45:07Z","date_created":"2018-12-11T11:53:02Z","date_published":"2015-10-20T00:00:00Z","_id":"1615","external_id":{"isi":["000363780000008"]},"citation":{"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.","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. <i>Cell Reports</i>. 2015;13(3):516-523. doi:<a href=\"https://doi.org/10.1016/j.celrep.2015.09.011\">10.1016/j.celrep.2015.09.011</a>","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. <i>Cell Reports</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.celrep.2015.09.011\">https://doi.org/10.1016/j.celrep.2015.09.011</a>","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.","ieee":"M. Hammer <i>et al.</i>, “Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism,” <i>Cell Reports</i>, vol. 13, no. 3. Cell Press, pp. 516–523, 2015.","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.” <i>Cell Reports</i>. Cell Press, 2015. <a href=\"https://doi.org/10.1016/j.celrep.2015.09.011\">https://doi.org/10.1016/j.celrep.2015.09.011</a>.","mla":"Hammer, Matthieu, et al. “Perturbed Hippocampal Synaptic Inhibition and γ-Oscillations in a Neuroligin-4 Knockout Mouse Model of Autism.” <i>Cell Reports</i>, vol. 13, no. 3, Cell Press, 2015, pp. 516–23, doi:<a href=\"https://doi.org/10.1016/j.celrep.2015.09.011\">10.1016/j.celrep.2015.09.011</a>."},"issue":"3","has_accepted_license":"1","isi":1,"publication_status":"published","department":[{"_id":"PeJo"}],"author":[{"first_name":"Matthieu","full_name":"Hammer, Matthieu","last_name":"Hammer"},{"last_name":"Krueger Burg","full_name":"Krueger Burg, Dilja","first_name":"Dilja"},{"last_name":"Tuffy","full_name":"Tuffy, Liam","first_name":"Liam"},{"last_name":"Cooper","full_name":"Cooper, Benjamin","first_name":"Benjamin"},{"last_name":"Taschenberger","full_name":"Taschenberger, Holger","first_name":"Holger"},{"id":"3A578F32-F248-11E8-B48F-1D18A9856A87","first_name":"Sarit","last_name":"Goswami","full_name":"Goswami, Sarit"},{"first_name":"Hannelore","full_name":"Ehrenreich, Hannelore","last_name":"Ehrenreich"},{"orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","first_name":"Peter M"},{"full_name":"Varoqueaux, Frederique","last_name":"Varoqueaux","first_name":"Frederique"},{"first_name":"Jeong","last_name":"Rhee","full_name":"Rhee, Jeong"},{"first_name":"Nils","last_name":"Brose","full_name":"Brose, Nils"}],"volume":13,"month":"10","intvolume":"        13","ddc":["570"],"scopus_import":"1","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.","language":[{"iso":"eng"}],"page":"516 - 523","oa_version":"Published Version","pubrep_id":"470"},{"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","type":"journal_article","publication":"Neuron","article_processing_charge":"No","day":"18","year":"2015","publist_id":"5256","file_date_updated":"2020-07-14T12:45:19Z","date_created":"2018-12-11T11:54:19Z","date_published":"2015-03-18T00:00:00Z","_id":"1845","external_id":{"isi":["000351319000002"]},"tmp":{"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)","image":"/images/cc_by_nc.png"},"oa":1,"status":"public","doi":"10.1016/j.neuron.2015.03.006","date_updated":"2025-09-23T08:44:39Z","publisher":"Elsevier","title":"Excitement about inhibitory presynaptic terminals","quality_controlled":"1","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."}],"file":[{"checksum":"d1808550e376a0eca2a950fda017cfa6","file_id":"5192","content_type":"application/pdf","date_updated":"2020-07-14T12:45:19Z","file_name":"IST-2017-822-v1+1_Perspective_Fig__Final.pdf","date_created":"2018-12-12T10:16:07Z","relation":"main_file","creator":"system","file_size":411832,"access_level":"open_access"},{"checksum":"a279f4ae61e6c8f33d68f69a0d02097d","content_type":"application/pdf","file_id":"5193","date_updated":"2020-07-14T12:45:19Z","file_name":"IST-2017-822-v1+2_Perspective_Final2.pdf","relation":"main_file","date_created":"2018-12-12T10:16:07Z","file_size":100769,"access_level":"open_access","creator":"system"}],"isi":1,"publication_status":"published","department":[{"_id":"PeJo"}],"author":[{"first_name":"David H","id":"3AE48E0A-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7577-1676","full_name":"Vandael, David H","last_name":"Vandael"},{"first_name":"Claudia ","id":"31FFEE2E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-4710-2082","last_name":"Espinoza Martinez","full_name":"Espinoza Martinez, Claudia "},{"first_name":"Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M","last_name":"Jonas"}],"volume":85,"month":"03","intvolume":"        85","ddc":["570"],"scopus_import":"1","language":[{"iso":"eng"}],"page":"1149 - 1151","oa_version":"Published Version","pubrep_id":"822","corr_author":"1","citation":{"ama":"Vandael DH, Espinoza Martinez C, Jonas PM. Excitement about inhibitory presynaptic terminals. <i>Neuron</i>. 2015;85(6):1149-1151. doi:<a href=\"https://doi.org/10.1016/j.neuron.2015.03.006\">10.1016/j.neuron.2015.03.006</a>","apa":"Vandael, D. H., Espinoza Martinez, C., &#38; Jonas, P. M. (2015). Excitement about inhibitory presynaptic terminals. <i>Neuron</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuron.2015.03.006\">https://doi.org/10.1016/j.neuron.2015.03.006</a>","short":"D.H. Vandael, C. Espinoza Martinez, P.M. Jonas, Neuron 85 (2015) 1149–1151.","chicago":"Vandael, David H, Claudia  Espinoza Martinez, and Peter M Jonas. “Excitement about Inhibitory Presynaptic Terminals.” <i>Neuron</i>. Elsevier, 2015. <a href=\"https://doi.org/10.1016/j.neuron.2015.03.006\">https://doi.org/10.1016/j.neuron.2015.03.006</a>.","ieee":"D. H. Vandael, C. Espinoza Martinez, and P. M. Jonas, “Excitement about inhibitory presynaptic terminals,” <i>Neuron</i>, vol. 85, no. 6. Elsevier, pp. 1149–1151, 2015.","mla":"Vandael, David H., et al. “Excitement about Inhibitory Presynaptic Terminals.” <i>Neuron</i>, vol. 85, no. 6, Elsevier, 2015, pp. 1149–51, doi:<a href=\"https://doi.org/10.1016/j.neuron.2015.03.006\">10.1016/j.neuron.2015.03.006</a>.","ista":"Vandael DH, Espinoza Martinez C, Jonas PM. 2015. Excitement about inhibitory presynaptic terminals. Neuron. 85(6), 1149–1151."},"issue":"6","has_accepted_license":"1"},{"publisher":"SAGE Publications","abstract":[{"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.","lang":"eng"}],"quality_controlled":"1","title":"Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats","file":[{"checksum":"53e16bd3fc2ae2c0d7de9164626c37aa","content_type":"application/pdf","file_id":"5057","date_updated":"2020-07-14T12:45:18Z","file_name":"IST-2016-456-v1+1_ASN_Neuro-2015-Chen-.pdf","relation":"main_file","date_created":"2018-12-12T10:14:08Z","access_level":"open_access","file_size":1146814,"creator":"system"}],"tmp":{"name":"Creative Commons Attribution 3.0 Unported (CC BY 3.0)","legal_code_url":"https://creativecommons.org/licenses/by/3.0/legalcode","image":"/images/cc_by.png","short":"CC BY (3.0)"},"article_type":"original","oa":1,"status":"public","doi":"10.1177/1759091415575845","date_updated":"2025-09-23T09:31:50Z","year":"2015","publist_id":"5269","file_date_updated":"2020-07-14T12:45:18Z","license":"https://creativecommons.org/licenses/by/3.0/","date_created":"2018-12-11T11:54:16Z","date_published":"2015-04-13T00:00:00Z","_id":"1834","external_id":{"isi":["000353223200002"]},"type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","publication":"ASN Neuro","article_processing_charge":"No","day":"13","citation":{"short":"C. Chen, C. Wang, X. Zhao, T. Zhou, D. Xu, Z. Wang, Y. Wang, ASN Neuro 7 (2015).","apa":"Chen, C., Wang, C., Zhao, X., Zhou, T., Xu, D., Wang, Z., &#38; Wang, Y. (2015). Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats. <i>ASN Neuro</i>. SAGE Publications. <a href=\"https://doi.org/10.1177/1759091415575845\">https://doi.org/10.1177/1759091415575845</a>","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. <i>ASN Neuro</i>. 2015;7(2). doi:<a href=\"https://doi.org/10.1177/1759091415575845\">10.1177/1759091415575845</a>","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.” <i>ASN Neuro</i>, vol. 7, no. 2, SAGE Publications, 2015, doi:<a href=\"https://doi.org/10.1177/1759091415575845\">10.1177/1759091415575845</a>.","ieee":"C. Chen <i>et al.</i>, “Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats,” <i>ASN Neuro</i>, vol. 7, no. 2. SAGE Publications, 2015.","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.” <i>ASN Neuro</i>. SAGE Publications, 2015. <a href=\"https://doi.org/10.1177/1759091415575845\">https://doi.org/10.1177/1759091415575845</a>."},"issue":"2","has_accepted_license":"1","language":[{"iso":"eng"}],"oa_version":"Published Version","pubrep_id":"456","publication_status":"published","isi":1,"author":[{"last_name":"Chen","full_name":"Chen, Chong","first_name":"Chong","id":"3DFD581A-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Wang, Chao","last_name":"Wang","first_name":"Chao"},{"full_name":"Zhao, Xuan","last_name":"Zhao","first_name":"Xuan"},{"first_name":"Tao","last_name":"Zhou","full_name":"Zhou, Tao"},{"last_name":"Xu","full_name":"Xu, Dao","first_name":"Dao"},{"first_name":"Zhi","full_name":"Wang, Zhi","last_name":"Wang"},{"last_name":"Wang","full_name":"Wang, Ying","first_name":"Ying"}],"department":[{"_id":"PeJo"}],"volume":7,"month":"04","ddc":["570"],"intvolume":"         7","scopus_import":"1"},{"date_published":"2014-03-23T00:00:00Z","external_id":{"isi":["000335016200012"]},"_id":"2228","date_created":"2018-12-11T11:56:26Z","year":"2014","publist_id":"4733","article_processing_charge":"No","day":"23","publication":"Nature Neuroscience","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","type":"journal_article","publisher":"Nature Publishing Group","quality_controlled":"1","abstract":[{"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.","lang":"eng"}],"title":"A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4286295/","open_access":"1"}],"publication_identifier":{"issn":["1097-6256"]},"project":[{"call_identifier":"FP7","_id":"25C0F108-B435-11E9-9278-68D0E5697425","grant_number":"268548","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons"},{"call_identifier":"FWF","name":"Mechanisms of transmitter release at GABAergic synapses","grant_number":"P24909-B24","_id":"25C26B1E-B435-11E9-9278-68D0E5697425"}],"status":"public","doi":"10.1038/nn.3678","date_updated":"2025-09-29T11:25:07Z","oa":1,"page":"686-693","oa_version":"Submitted Version","language":[{"iso":"eng"}],"intvolume":"        17","scopus_import":"1","volume":17,"month":"03","isi":1,"publication_status":"published","author":[{"id":"4AC0145C-F248-11E8-B48F-1D18A9856A87","first_name":"Hua","last_name":"Hu","full_name":"Hu, Hua"},{"id":"353C1B58-F248-11E8-B48F-1D18A9856A87","first_name":"Peter M","orcid":"0000-0001-5001-4804","last_name":"Jonas","full_name":"Jonas, Peter M"}],"department":[{"_id":"PeJo"}],"ec_funded":1,"issue":"5","corr_author":"1","citation":{"short":"H. Hu, P.M. Jonas, Nature Neuroscience 17 (2014) 686–693.","apa":"Hu, H., &#38; Jonas, P. M. (2014). A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons. <i>Nature Neuroscience</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/nn.3678\">https://doi.org/10.1038/nn.3678</a>","ama":"Hu H, Jonas PM. A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons. <i>Nature Neuroscience</i>. 2014;17(5):686-693. doi:<a href=\"https://doi.org/10.1038/nn.3678\">10.1038/nn.3678</a>","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.” <i>Nature Neuroscience</i>, vol. 17, no. 5, Nature Publishing Group, 2014, pp. 686–93, doi:<a href=\"https://doi.org/10.1038/nn.3678\">10.1038/nn.3678</a>.","chicago":"Hu, Hua, and Peter M Jonas. “A Supercritical Density of Na^+ Channels Ensures Fast Signaling in GABAergic Interneuron Axons.” <i>Nature Neuroscience</i>. Nature Publishing Group, 2014. <a href=\"https://doi.org/10.1038/nn.3678\">https://doi.org/10.1038/nn.3678</a>.","ieee":"H. Hu and P. M. Jonas, “A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons,” <i>Nature Neuroscience</i>, vol. 17, no. 5. Nature Publishing Group, pp. 686–693, 2014."}},{"status":"public","date_updated":"2025-09-29T11:24:38Z","doi":"10.1126/science.1244811","project":[{"call_identifier":"FWF","_id":"25C26B1E-B435-11E9-9278-68D0E5697425","grant_number":"P24909-B24","name":"Mechanisms of transmitter release at GABAergic synapses"},{"_id":"25C0F108-B435-11E9-9278-68D0E5697425","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","grant_number":"268548","call_identifier":"FP7"}],"oa":1,"abstract":[{"text":"The distance between Ca^2+ channels and release sensors determines the speed and efficacy of synaptic transmission. Tight &quot;nanodomain&quot; channel-sensor coupling initiates transmitter release at synapses in the mature brain, whereas loose &quot;microdomain&quot; 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.","lang":"eng"}],"title":"Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse","quality_controlled":"1","publisher":"American Association for the Advancement of Science","main_file_link":[{"open_access":"1","url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617475/"}],"publication_identifier":{"issn":["0036-8075"]},"day":"01","article_processing_charge":"No","publication":"Science","type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","external_id":{"isi":["000330724000044"]},"_id":"2229","date_published":"2014-02-01T00:00:00Z","date_created":"2018-12-11T11:56:27Z","publist_id":"4732","year":"2014","ec_funded":1,"issue":"6171","citation":{"short":"N. Vyleta, P.M. Jonas, Science 343 (2014) 665–670.","ama":"Vyleta N, Jonas PM. Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse. <i>Science</i>. 2014;343(6171):665-670. doi:<a href=\"https://doi.org/10.1126/science.1244811\">10.1126/science.1244811</a>","apa":"Vyleta, N., &#38; Jonas, P. M. (2014). Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse. <i>Science</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/science.1244811\">https://doi.org/10.1126/science.1244811</a>","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.","chicago":"Vyleta, Nicholas, and Peter M Jonas. “Loose Coupling between Ca^2+ Channels and Release Sensors at a Plastic Hippocampal Synapse.” <i>Science</i>. American Association for the Advancement of Science, 2014. <a href=\"https://doi.org/10.1126/science.1244811\">https://doi.org/10.1126/science.1244811</a>.","ieee":"N. Vyleta and P. M. Jonas, “Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse,” <i>Science</i>, vol. 343, no. 6171. American Association for the Advancement of Science, pp. 665–670, 2014.","mla":"Vyleta, Nicholas, and Peter M. Jonas. “Loose Coupling between Ca^2+ Channels and Release Sensors at a Plastic Hippocampal Synapse.” <i>Science</i>, vol. 343, no. 6171, American Association for the Advancement of Science, 2014, pp. 665–70, doi:<a href=\"https://doi.org/10.1126/science.1244811\">10.1126/science.1244811</a>."},"corr_author":"1","scopus_import":"1","intvolume":"       343","volume":343,"month":"02","department":[{"_id":"PeJo"}],"author":[{"id":"36C4978E-F248-11E8-B48F-1D18A9856A87","first_name":"Nicholas","last_name":"Vyleta","full_name":"Vyleta, Nicholas"},{"id":"353C1B58-F248-11E8-B48F-1D18A9856A87","first_name":"Peter M","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M","last_name":"Jonas"}],"isi":1,"publication_status":"published","oa_version":"Submitted Version","page":"665 - 670","language":[{"iso":"eng"}]},{"citation":{"short":"J. Guzmán, A. Schlögl, C. Schmidt Hieber, Frontiers in Neuroinformatics 8 (2014).","apa":"Guzmán, J., Schlögl, A., &#38; Schmidt Hieber, C. (2014). Stimfit: Quantifying electrophysiological data with Python. <i>Frontiers in Neuroinformatics</i>. Frontiers Research Foundation. <a href=\"https://doi.org/10.3389/fninf.2014.00016\">https://doi.org/10.3389/fninf.2014.00016</a>","ama":"Guzmán J, Schlögl A, Schmidt Hieber C. Stimfit: Quantifying electrophysiological data with Python. <i>Frontiers in Neuroinformatics</i>. 2014;8(FEB). doi:<a href=\"https://doi.org/10.3389/fninf.2014.00016\">10.3389/fninf.2014.00016</a>","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.” <i>Frontiers in Neuroinformatics</i>, vol. 8, no. FEB, 16, Frontiers Research Foundation, 2014, doi:<a href=\"https://doi.org/10.3389/fninf.2014.00016\">10.3389/fninf.2014.00016</a>.","ieee":"J. Guzmán, A. Schlögl, and C. Schmidt Hieber, “Stimfit: Quantifying electrophysiological data with Python,” <i>Frontiers in Neuroinformatics</i>, vol. 8, no. FEB. Frontiers Research Foundation, 2014.","chicago":"Guzmán, José, Alois Schlögl, and Christoph Schmidt Hieber. “Stimfit: Quantifying Electrophysiological Data with Python.” <i>Frontiers in Neuroinformatics</i>. Frontiers Research Foundation, 2014. <a href=\"https://doi.org/10.3389/fninf.2014.00016\">https://doi.org/10.3389/fninf.2014.00016</a>."},"article_number":"16","issue":"FEB","has_accepted_license":"1","language":[{"iso":"eng"}],"oa_version":"Published Version","pubrep_id":"425","author":[{"first_name":"José","id":"30CC5506-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2209-5242","full_name":"Guzmán, José","last_name":"Guzmán"},{"id":"45BF87EE-F248-11E8-B48F-1D18A9856A87","first_name":"Alois","last_name":"Schlögl","full_name":"Schlögl, Alois","orcid":"0000-0002-5621-8100"},{"full_name":"Schmidt Hieber, Christoph","last_name":"Schmidt Hieber","first_name":"Christoph"}],"department":[{"_id":"ScienComp"},{"_id":"PeJo"}],"isi":1,"publication_status":"published","volume":8,"month":"02","scopus_import":"1","intvolume":"         8","ddc":["570"],"publication_identifier":{"issn":["1662-5196"]},"title":"Stimfit: Quantifying electrophysiological data with Python","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."}],"quality_controlled":"1","publisher":"Frontiers Research Foundation","file":[{"date_created":"2018-12-12T10:12:17Z","relation":"main_file","file_size":2883372,"creator":"system","access_level":"open_access","file_name":"IST-2016-425-v1+1_fninf-08-00016.pdf","date_updated":"2020-07-14T12:45:34Z","file_id":"4935","checksum":"eeca00bba7232ff7d27db83321f6ea30","content_type":"application/pdf"}],"tmp":{"image":"/images/cc_by.png","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"oa":1,"doi":"10.3389/fninf.2014.00016","status":"public","date_updated":"2025-09-29T11:24:02Z","publist_id":"4731","year":"2014","file_date_updated":"2020-07-14T12:45:34Z","date_created":"2018-12-11T11:56:27Z","_id":"2230","external_id":{"isi":["000348105900001"]},"date_published":"2014-02-21T00:00:00Z","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","type":"journal_article","publication":"Frontiers in Neuroinformatics","day":"21","article_processing_charge":"No"},{"file":[{"date_updated":"2020-07-14T12:45:35Z","checksum":"438547cfcd9045a22f065f2019f07849","file_id":"4773","content_type":"application/pdf","creator":"system","file_size":4373072,"access_level":"open_access","relation":"main_file","date_created":"2018-12-12T10:09:48Z","file_name":"IST-2016-422-v1+1_1-s2.0-S0896627313009227-main.pdf"}],"quality_controlled":"1","abstract":[{"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.","lang":"eng"}],"title":"Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations","publisher":"Elsevier","publication_identifier":{"issn":["0896-6273"]},"doi":"10.1016/j.neuron.2013.09.046","date_updated":"2026-04-16T10:08:53Z","status":"public","project":[{"name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","grant_number":"268548","_id":"25C0F108-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"},{"name":"Mechanisms of transmitter release at GABAergic synapses","grant_number":"P24909-B24","_id":"25C26B1E-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"}],"oa":1,"external_id":{"isi":["000329559000015"]},"_id":"2254","date_published":"2014-01-08T00:00:00Z","date_created":"2018-12-11T11:56:35Z","file_date_updated":"2020-07-14T12:45:35Z","publist_id":"4692","year":"2014","day":"08","article_processing_charge":"No","publication":"Neuron","user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","type":"journal_article","ec_funded":1,"has_accepted_license":"1","issue":"1","citation":{"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.” <i>Neuron</i>, vol. 81, no. 1, Elsevier, 2014, pp. 140–52, doi:<a href=\"https://doi.org/10.1016/j.neuron.2013.09.046\">10.1016/j.neuron.2013.09.046</a>.","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.” <i>Neuron</i>. Elsevier, 2014. <a href=\"https://doi.org/10.1016/j.neuron.2013.09.046\">https://doi.org/10.1016/j.neuron.2013.09.046</a>.","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,” <i>Neuron</i>, vol. 81, no. 1. Elsevier, pp. 140–152, 2014.","short":"A. Pernia-Andrade, P.M. Jonas, Neuron 81 (2014) 140–152.","apa":"Pernia-Andrade, A., &#38; Jonas, P. M. (2014). Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations. <i>Neuron</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuron.2013.09.046\">https://doi.org/10.1016/j.neuron.2013.09.046</a>","ama":"Pernia-Andrade A, Jonas PM. Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations. <i>Neuron</i>. 2014;81(1):140-152. doi:<a href=\"https://doi.org/10.1016/j.neuron.2013.09.046\">10.1016/j.neuron.2013.09.046</a>"},"corr_author":"1","pubrep_id":"422","oa_version":"Published Version","page":"140 - 152","language":[{"iso":"eng"}],"scopus_import":"1","intvolume":"        81","ddc":["570"],"month":"01","volume":81,"department":[{"_id":"PeJo"}],"author":[{"last_name":"Pernia-Andrade","full_name":"Pernia-Andrade, Alejandro","first_name":"Alejandro","id":"36963E98-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804","last_name":"Jonas","full_name":"Jonas, Peter M"}],"isi":1,"publication_status":"published"},{"has_accepted_license":"1","citation":{"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.” <i>Hippocampus</i>, vol. 23, no. 2, Wiley-Blackwell, 2014, pp. 189–203, doi:<a href=\"https://doi.org/10.1002/hipo.22214\">10.1002/hipo.22214</a>.","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.” <i>Hippocampus</i>. Wiley-Blackwell, 2014. <a href=\"https://doi.org/10.1002/hipo.22214\">https://doi.org/10.1002/hipo.22214</a>.","ieee":"J. Hosp <i>et al.</i>, “Morpho-physiological criteria divide dentate gyrus interneurons into classes,” <i>Hippocampus</i>, vol. 23, no. 2. Wiley-Blackwell, pp. 189–203, 2014.","short":"J. Hosp, M. Strüber, Y. Yanagawa, K. Obata, I. Vida, P.M. Jonas, M. Bartos, Hippocampus 23 (2014) 189–203.","apa":"Hosp, J., Strüber, M., Yanagawa, Y., Obata, K., Vida, I., Jonas, P. M., &#38; Bartos, M. (2014). Morpho-physiological criteria divide dentate gyrus interneurons into classes. <i>Hippocampus</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1002/hipo.22214\">https://doi.org/10.1002/hipo.22214</a>","ama":"Hosp J, Strüber M, Yanagawa Y, et al. Morpho-physiological criteria divide dentate gyrus interneurons into classes. <i>Hippocampus</i>. 2014;23(2):189-203. doi:<a href=\"https://doi.org/10.1002/hipo.22214\">10.1002/hipo.22214</a>"},"issue":"2","scopus_import":"1","ddc":["570"],"intvolume":"        23","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.","department":[{"_id":"PeJo"}],"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"},{"full_name":"Vida, Imre","last_name":"Vida","first_name":"Imre"},{"orcid":"0000-0001-5001-4804","last_name":"Jonas","full_name":"Jonas, Peter M","first_name":"Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Bartos","full_name":"Bartos, Marlene","first_name":"Marlene"}],"publication_status":"published","isi":1,"volume":23,"month":"02","pubrep_id":"461","language":[{"iso":"eng"}],"oa_version":"Published Version","page":"189 - 203","status":"public","doi":"10.1002/hipo.22214","date_updated":"2025-09-29T11:11:47Z","tmp":{"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)","image":"/images/cc_by_nc.png"},"oa":1,"title":"Morpho-physiological criteria divide dentate gyrus interneurons into classes","quality_controlled":"1","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."}],"publisher":"Wiley-Blackwell","file":[{"creator":"system","file_size":801589,"access_level":"open_access","date_created":"2018-12-12T10:15:54Z","relation":"main_file","file_name":"IST-2016-461-v1+1_Hosp_et_al-2014-Hippocampus.pdf","date_updated":"2020-07-14T12:45:37Z","file_id":"5178","checksum":"ff6bc75a79dbc985a2e31b79253e6444","content_type":"application/pdf"}],"day":"01","article_processing_charge":"No","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","type":"journal_article","publication":"Hippocampus","date_created":"2018-12-11T11:56:46Z","external_id":{"isi":["000329879300006"]},"_id":"2285","date_published":"2014-02-01T00:00:00Z","publist_id":"4646","year":"2014","file_date_updated":"2020-07-14T12:45:37Z"},{"issue":"8","citation":{"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.","apa":"Chai, X., Münzner, G., Zhao, S., Tinnes, S., Kowalski, J., Häussler, U., … Frotscher, M. (2014). Epilepsy-induced motility of differentiated neurons. <i>Cerebral Cortex</i>. Oxford University Press. <a href=\"https://doi.org/10.1093/cercor/bht067\">https://doi.org/10.1093/cercor/bht067</a>","ama":"Chai X, Münzner G, Zhao S, et al. Epilepsy-induced motility of differentiated neurons. <i>Cerebral Cortex</i>. 2014;24(8):2130-2140. doi:<a href=\"https://doi.org/10.1093/cercor/bht067\">10.1093/cercor/bht067</a>","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.” <i>Cerebral Cortex</i>, vol. 24, no. 8, Oxford University Press, 2014, pp. 2130–40, doi:<a href=\"https://doi.org/10.1093/cercor/bht067\">10.1093/cercor/bht067</a>.","ieee":"X. Chai <i>et al.</i>, “Epilepsy-induced motility of differentiated neurons,” <i>Cerebral Cortex</i>, vol. 24, no. 8. Oxford University Press, pp. 2130–2140, 2014.","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.” <i>Cerebral Cortex</i>. Oxford University Press, 2014. <a href=\"https://doi.org/10.1093/cercor/bht067\">https://doi.org/10.1093/cercor/bht067</a>."},"oa_version":"None","page":"2130 - 2140","language":[{"iso":"eng"}],"month":"08","volume":24,"department":[{"_id":"PeJo"}],"author":[{"first_name":"Xuejun","last_name":"Chai","full_name":"Chai, Xuejun"},{"full_name":"Münzner, Gert","last_name":"Münzner","first_name":"Gert"},{"first_name":"Shanting","last_name":"Zhao","full_name":"Zhao, Shanting"},{"last_name":"Tinnes","full_name":"Tinnes, Stefanie","first_name":"Stefanie"},{"id":"3F3CA136-F248-11E8-B48F-1D18A9856A87","first_name":"Janina","last_name":"Kowalski","full_name":"Kowalski, Janina"},{"last_name":"Häussler","full_name":"Häussler, Ute","first_name":"Ute"},{"first_name":"Christina","full_name":"Young, Christina","last_name":"Young"},{"first_name":"Carola","full_name":"Haas, Carola","last_name":"Haas"},{"last_name":"Frotscher","full_name":"Frotscher, Michael","first_name":"Michael"}],"isi":1,"publication_status":"published","scopus_import":"1","intvolume":"        24","quality_controlled":"1","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. "}],"title":"Epilepsy-induced motility of differentiated neurons","publisher":"Oxford University Press","date_updated":"2025-09-29T11:41:17Z","doi":"10.1093/cercor/bht067","status":"public","publist_id":"4820","year":"2014","external_id":{"isi":["000340068500014"]},"_id":"2164","date_published":"2014-08-01T00:00:00Z","date_created":"2018-12-11T11:56:04Z","publication":"Cerebral Cortex","type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","day":"01","article_processing_charge":"No"},{"project":[{"_id":"25BDE9A4-B435-11E9-9278-68D0E5697425","name":"Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen","grant_number":"SFB-TR3-TP10B"}],"doi":"10.1038/nprot.2014.099","date_updated":"2025-09-29T11:36:43Z","status":"public","publisher":"Nature Publishing Group","quality_controlled":"1","abstract":[{"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.","lang":"eng"}],"title":"Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue","article_processing_charge":"No","day":"29","publication":"Nature Protocols","type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","date_published":"2014-05-29T00:00:00Z","external_id":{"isi":["000337145800020"]},"_id":"2176","date_created":"2018-12-11T11:56:09Z","year":"2014","publist_id":"4807","issue":"6","citation":{"short":"D. Studer, S. Zhao, X. Chai, P.M. Jonas, W. Graber, S. Nestel, M. Frotscher, Nature Protocols 9 (2014) 1480–1495.","ama":"Studer D, Zhao S, Chai X, et al. Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue. <i>Nature Protocols</i>. 2014;9(6):1480-1495. doi:<a href=\"https://doi.org/10.1038/nprot.2014.099\">10.1038/nprot.2014.099</a>","apa":"Studer, D., Zhao, S., Chai, X., Jonas, P. M., Graber, W., Nestel, S., &#38; Frotscher, M. (2014). Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue. <i>Nature Protocols</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/nprot.2014.099\">https://doi.org/10.1038/nprot.2014.099</a>","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.","ieee":"D. Studer <i>et al.</i>, “Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue,” <i>Nature Protocols</i>, vol. 9, no. 6. Nature Publishing Group, pp. 1480–1495, 2014.","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.” <i>Nature Protocols</i>. Nature Publishing Group, 2014. <a href=\"https://doi.org/10.1038/nprot.2014.099\">https://doi.org/10.1038/nprot.2014.099</a>.","mla":"Studer, Daniel, et al. “Capture of Activity-Induced Ultrastructural Changes at Synapses by High-Pressure Freezing of Brain Tissue.” <i>Nature Protocols</i>, vol. 9, no. 6, Nature Publishing Group, 2014, pp. 1480–95, doi:<a href=\"https://doi.org/10.1038/nprot.2014.099\">10.1038/nprot.2014.099</a>."},"intvolume":"         9","scopus_import":"1","month":"05","volume":9,"isi":1,"publication_status":"published","department":[{"_id":"PeJo"}],"author":[{"last_name":"Studer","full_name":"Studer, Daniel","first_name":"Daniel"},{"first_name":"Shanting","last_name":"Zhao","full_name":"Zhao, Shanting"},{"first_name":"Xuejun","full_name":"Chai, Xuejun","last_name":"Chai"},{"first_name":"Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","last_name":"Jonas","full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804"},{"first_name":"Werner","full_name":"Graber, Werner","last_name":"Graber"},{"last_name":"Nestel","full_name":"Nestel, Sigrun","first_name":"Sigrun"},{"last_name":"Frotscher","full_name":"Frotscher, Michael","first_name":"Michael"}],"page":"1480 - 1495","oa_version":"None","language":[{"iso":"eng"}]}]