[{"type":"journal_article","day":"07","status":"public","intvolume":"        43","file_date_updated":"2023-07-10T09:04:58Z","page":"4197-4216","publication":"The Journal of Neuroscience","issue":"23","date_published":"2023-06-07T00:00:00Z","article_type":"original","month":"06","language":[{"iso":"eng"}],"scopus_import":"1","publisher":"Society for Neuroscience","department":[{"_id":"RySh"}],"has_accepted_license":"1","file":[{"success":1,"relation":"main_file","content_type":"application/pdf","creator":"alisjak","file_id":"13205","file_size":7794425,"file_name":"2023_JN_Eguchi.pdf","checksum":"70b2141870e0bf1c94fd343e18fdbc32","date_created":"2023-07-10T09:04:58Z","access_level":"open_access","date_updated":"2023-07-10T09:04:58Z"}],"date_created":"2023-07-09T22:01:12Z","citation":{"apa":"Eguchi, K., Le Monnier, E., &#38; Shigemoto, R. (2023). Nanoscale phosphoinositide distribution on cell membranes of mouse cerebellar neurons. <i>The Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.1514-22.2023\">https://doi.org/10.1523/JNEUROSCI.1514-22.2023</a>","ieee":"K. Eguchi, E. Le Monnier, and R. Shigemoto, “Nanoscale phosphoinositide distribution on cell membranes of mouse cerebellar neurons,” <i>The Journal of Neuroscience</i>, vol. 43, no. 23. Society for Neuroscience, pp. 4197–4216, 2023.","chicago":"Eguchi, Kohgaku, Elodie Le Monnier, and Ryuichi Shigemoto. “Nanoscale Phosphoinositide Distribution on Cell Membranes of Mouse Cerebellar Neurons.” <i>The Journal of Neuroscience</i>. Society for Neuroscience, 2023. <a href=\"https://doi.org/10.1523/JNEUROSCI.1514-22.2023\">https://doi.org/10.1523/JNEUROSCI.1514-22.2023</a>.","mla":"Eguchi, Kohgaku, et al. “Nanoscale Phosphoinositide Distribution on Cell Membranes of Mouse Cerebellar Neurons.” <i>The Journal of Neuroscience</i>, vol. 43, no. 23, Society for Neuroscience, 2023, pp. 4197–216, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.1514-22.2023\">10.1523/JNEUROSCI.1514-22.2023</a>.","ama":"Eguchi K, Le Monnier E, Shigemoto R. Nanoscale phosphoinositide distribution on cell membranes of mouse cerebellar neurons. <i>The Journal of Neuroscience</i>. 2023;43(23):4197-4216. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.1514-22.2023\">10.1523/JNEUROSCI.1514-22.2023</a>","ista":"Eguchi K, Le Monnier E, Shigemoto R. 2023. Nanoscale phosphoinositide distribution on cell membranes of mouse cerebellar neurons. The Journal of Neuroscience. 43(23), 4197–4216.","short":"K. Eguchi, E. Le Monnier, R. Shigemoto, The Journal of Neuroscience 43 (2023) 4197–4216."},"publication_status":"published","author":[{"first_name":"Kohgaku","full_name":"Eguchi, Kohgaku","last_name":"Eguchi","orcid":"0000-0002-6170-2546","id":"2B7846DC-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Elodie","full_name":"Le Monnier, Elodie","last_name":"Le Monnier","id":"3B59276A-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Shigemoto","full_name":"Shigemoto, Ryuichi","orcid":"0000-0001-8761-9444","first_name":"Ryuichi","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87"}],"abstract":[{"text":"Phosphatidylinositol-4,5-bisphosphate (PI(4,5)P2) plays an essential role in neuronal activities through interaction with various proteins involved in signaling at membranes. However, the distribution pattern of PI(4,5)P2 and the association with these proteins on the neuronal cell membranes remain elusive. In this study, we established a method for visualizing PI(4,5)P2 by SDS-digested freeze-fracture replica labeling (SDS-FRL) to investigate the quantitative nanoscale distribution of PI(4,5)P2 in cryo-fixed brain. We demonstrate that PI(4,5)P2 forms tiny clusters with a mean size of ∼1000 nm2 rather than randomly distributed in cerebellar neuronal membranes in male C57BL/6J mice. These clusters show preferential accumulation in specific membrane compartments of different cell types, in particular, in Purkinje cell (PC) spines and granule cell (GC) presynaptic active zones. Furthermore, we revealed extensive association of PI(4,5)P2 with CaV2.1 and GIRK3 across different membrane compartments, whereas its association with mGluR1α was compartment specific. These results suggest that our SDS-FRL method provides valuable insights into the physiological functions of PI(4,5)P2 in neurons.","lang":"eng"}],"article_processing_charge":"No","volume":43,"oa":1,"date_updated":"2023-10-18T07:12:47Z","project":[{"_id":"2659CC84-B435-11E9-9278-68D0E5697425","name":"Ultrastructural analysis of phosphoinositides in nerve terminals: distribution, dynamics and physiological roles in synaptic transmission","call_identifier":"H2020","grant_number":"793482"},{"_id":"25CA28EA-B435-11E9-9278-68D0E5697425","name":"In situ analysis of single channel subunit composition in neurons: physiological implication in synaptic plasticity and behaviour","call_identifier":"H2020","grant_number":"694539"}],"quality_controlled":"1","oa_version":"Published Version","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","acknowledgement":"This work was supported by The Institute of Science and Technology (IST) Austria, the European Union's Horizon 2020 Research and Innovation Program under the Marie Skłodowska-Curie Grant Agreement No. 793482 (to K.E.) and by the European Research Council (ERC) Grant Agreement No. 694539 (to R.S.). We thank Nicoleta Condruz (IST Austria, Klosterneuburg, Austria) for technical assistance with sample preparation, the Electron Microscopy Facility of IST Austria (Klosterneuburg, Austria) for technical support with EM works, Natalia Baranova (University of Vienna, Vienna, Austria) and Martin Loose (IST Austria, Klosterneuburg, Austria) for advice on liposome preparation, and Yugo Fukazawa (University of Fukui, Fukui, Japan) for comments.","publication_identifier":{"eissn":["1529-2401"],"issn":["0270-6474"]},"pmid":1,"_id":"13202","ec_funded":1,"doi":"10.1523/JNEUROSCI.1514-22.2023","year":"2023","acknowledged_ssus":[{"_id":"EM-Fac"}],"title":"Nanoscale phosphoinositide distribution on cell membranes of mouse cerebellar neurons","external_id":{"pmid":["37160366"],"isi":["001020132100005"]},"isi":1,"tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"ddc":["570"]},{"publication_identifier":{"eissn":["1529-2401"],"issn":["0270-6474"]},"pmid":1,"_id":"9073","quality_controlled":"1","oa_version":"Published Version","project":[{"grant_number":"725780","call_identifier":"H2020","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","_id":"260018B0-B435-11E9-9278-68D0E5697425"},{"grant_number":"F07805","_id":"059F6AB4-7A3F-11EA-A408-12923DDC885E","name":"Molecular Mechanisms of Neural Stem Cell Lineage Progression"}],"acknowledgement":"Work in the I.L.H.-O. laboratory was supported by European Research Council Grant ERC-2015-CoG 681577 and German Research Foundation Ha 4466/10-1, Ha4466/11-1, Ha4466/12-1, SPP 1665, and SFB 936B5. Work in the S.J.B.B. laboratory was supported by Biotechnology and Biological Sciences Research Council BB/P003796/1, Medical Research Council MR/K004387/1 and MR/T033320/1, Wellcome Trust 215199/Z/19/Z and 102386/Z/13/Z, and John Fell Fund. Work in the S.H. laboratory was supported by European Research Council Grants ERC-2016-CoG 725780 LinPro and FWF SFB F78. This work was supported by National Institutes of Health Grant NIMH 1R01MH110553 to N.V.D.M.G. Work in the J.A.C. laboratory was supported by the Ludwig Family Foundation, Simons Foundation SFARI Research Award, and National Institutes of Health/National Institute of Mental Health R01 MH102365 and R01MH113852. The B.V. laboratory was supported by Whitehall Foundation 2017-12-73, National Science Foundation 1736028, National Institutes of Health, National Institute of General Medical Sciences R01GM134363-01, and Halıcıoğlu Data Science Institute Fellowship. This work was supported by the University of California San Diego School of Medicine.","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","article_processing_charge":"No","date_updated":"2023-09-05T14:03:17Z","oa":1,"volume":41,"abstract":[{"lang":"eng","text":"The sensory and cognitive abilities of the mammalian neocortex are underpinned by intricate columnar and laminar circuits formed from an array of diverse neuronal populations. One approach to determining how interactions between these circuit components give rise to complex behavior is to investigate the rules by which cortical circuits are formed and acquire functionality during development. This review summarizes recent research on the development of the neocortex, from genetic determination in neural stem cells through to the dynamic role that specific neuronal populations play in the earliest circuits of neocortex, and how they contribute to emergent function and cognition. While many of these endeavors take advantage of model systems, consideration will also be given to advances in our understanding of activity in nascent human circuits. Such cross-species perspective is imperative when investigating the mechanisms underlying the dysfunction of early neocortical circuits in neurodevelopmental disorders, so that one can identify targets amenable to therapeutic intervention."}],"keyword":["General Neuroscience"],"author":[{"first_name":"Ileana L.","last_name":"Hanganu-Opatz","full_name":"Hanganu-Opatz, Ileana L."},{"last_name":"Butt","full_name":"Butt, Simon J. B.","first_name":"Simon J. B."},{"orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"},{"last_name":"De Marco García","full_name":"De Marco García, Natalia V.","first_name":"Natalia V."},{"last_name":"Cardin","full_name":"Cardin, Jessica A.","first_name":"Jessica A."},{"last_name":"Voytek","full_name":"Voytek, Bradley","first_name":"Bradley"},{"full_name":"Muotri, Alysson R.","last_name":"Muotri","first_name":"Alysson R."}],"citation":{"mla":"Hanganu-Opatz, Ileana L., et al. “The Logic of Developing Neocortical Circuits in Health and Disease.” <i>The Journal of Neuroscience</i>, vol. 41, no. 5, Society for Neuroscience, 2021, pp. 813–22, doi:<a href=\"https://doi.org/10.1523/jneurosci.1655-20.2020\">10.1523/jneurosci.1655-20.2020</a>.","ama":"Hanganu-Opatz IL, Butt SJB, Hippenmeyer S, et al. The logic of developing neocortical circuits in health and disease. <i>The Journal of Neuroscience</i>. 2021;41(5):813-822. doi:<a href=\"https://doi.org/10.1523/jneurosci.1655-20.2020\">10.1523/jneurosci.1655-20.2020</a>","ista":"Hanganu-Opatz IL, Butt SJB, Hippenmeyer S, De Marco García NV, Cardin JA, Voytek B, Muotri AR. 2021. The logic of developing neocortical circuits in health and disease. The Journal of Neuroscience. 41(5), 813–822.","short":"I.L. Hanganu-Opatz, S.J.B. Butt, S. Hippenmeyer, N.V. De Marco García, J.A. Cardin, B. Voytek, A.R. Muotri, The Journal of Neuroscience 41 (2021) 813–822.","ieee":"I. L. Hanganu-Opatz <i>et al.</i>, “The logic of developing neocortical circuits in health and disease,” <i>The Journal of Neuroscience</i>, vol. 41, no. 5. Society for Neuroscience, pp. 813–822, 2021.","apa":"Hanganu-Opatz, I. L., Butt, S. J. B., Hippenmeyer, S., De Marco García, N. V., Cardin, J. A., Voytek, B., &#38; Muotri, A. R. (2021). The logic of developing neocortical circuits in health and disease. <i>The Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/jneurosci.1655-20.2020\">https://doi.org/10.1523/jneurosci.1655-20.2020</a>","chicago":"Hanganu-Opatz, Ileana L., Simon J. B. Butt, Simon Hippenmeyer, Natalia V. De Marco García, Jessica A. Cardin, Bradley Voytek, and Alysson R. Muotri. “The Logic of Developing Neocortical Circuits in Health and Disease.” <i>The Journal of Neuroscience</i>. Society for Neuroscience, 2021. <a href=\"https://doi.org/10.1523/jneurosci.1655-20.2020\">https://doi.org/10.1523/jneurosci.1655-20.2020</a>."},"publication_status":"published","ddc":["570"],"isi":1,"external_id":{"isi":["000616763400002"],"pmid":["33431633"]},"title":"The logic of developing neocortical circuits in health and disease","year":"2021","doi":"10.1523/jneurosci.1655-20.2020","ec_funded":1,"publication":"The Journal of Neuroscience","issue":"5","file_date_updated":"2022-05-27T06:59:55Z","page":"813-822","intvolume":"        41","status":"public","day":"03","type":"journal_article","file":[{"date_updated":"2022-05-27T06:59:55Z","access_level":"open_access","date_created":"2022-05-27T06:59:55Z","checksum":"578fd7ed1a0aef74bce61bea2d987b33","file_name":"2021_JourNeuroscience_Hanganu.pdf","file_size":1031150,"file_id":"11414","creator":"dernst","content_type":"application/pdf","relation":"main_file","success":1}],"date_created":"2021-02-03T12:23:51Z","has_accepted_license":"1","department":[{"_id":"SiHi"}],"scopus_import":"1","publisher":"Society for Neuroscience","language":[{"iso":"eng"}],"month":"02","article_type":"original","date_published":"2021-02-03T00:00:00Z"},{"title":"RIM-binding protein 2 organizes Ca<sup>21</sup> channel topography and regulates release probability and vesicle replenishment at a fast central synapse","external_id":{"isi":["000752287700005"],"pmid":["34353898"]},"year":"2021","doi":"10.1523/JNEUROSCI.0586-21.2021","ddc":["570"],"tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"isi":1,"abstract":[{"text":"Rab-interacting molecule (RIM)-binding protein 2 (BP2) is a multidomain protein of the presynaptic active zone (AZ). By binding to RIM, bassoon (Bsn), and voltage-gated Ca2+ channels (CaV), it is considered to be a central organizer of the topography of CaV and release sites of synaptic vesicles (SVs) at the AZ. Here, we used RIM-BP2 knock-out (KO) mice and their wild-type (WT) littermates of either sex to investigate the role of RIM-BP2 at the endbulb of Held synapse of auditory nerve fibers (ANFs) with bushy cells (BCs) of the cochlear nucleus, a fast relay of the auditory pathway with high release probability. Disruption of RIM-BP2 lowered release probability altering short-term plasticity and reduced evoked EPSCs. Analysis of SV pool dynamics during high-frequency train stimulation indicated a reduction of SVs with high release probability but an overall normal size of the readily releasable SV pool (RRP). The Ca2+-dependent fast component of SV replenishment after RRP depletion was slowed. Ultrastructural analysis by superresolution light and electron microscopy revealed an impaired topography of presynaptic CaV and a reduction of docked and membrane-proximal SVs at the AZ. We conclude that RIM-BP2 organizes the topography of CaV, and promotes SV tethering and docking. This way RIM-BP2 is critical for establishing a high initial release probability as required to reliably signal sound onset information that we found to be degraded in BCs of RIM-BP2-deficient mice in vivo. SIGNIFICANCE STATEMENT: Rab-interacting molecule (RIM)-binding proteins (BPs) are key organizers of the active zone (AZ). Using a multidisciplinary approach to the calyceal endbulb of Held synapse that transmits auditory information at rates of up to hundreds of Hertz with submillisecond precision we demonstrate a requirement for RIM-BP2 for normal auditory signaling. Endbulb synapses lacking RIM-BP2 show a reduced release probability despite normal whole-terminal Ca2+ influx and abundance of the key priming protein Munc13-1, a reduced rate of SV replenishment, as well as an altered topography of voltage-gated (CaV)2.1 Ca2+ channels, and fewer docked and membrane proximal synaptic vesicles (SVs). This hampers transmission of sound onset information likely affecting downstream neural computations such as of sound localization.","lang":"eng"}],"author":[{"last_name":"Butola","full_name":"Butola, Tanvi","first_name":"Tanvi"},{"first_name":"Theocharis","full_name":"Alvanos, Theocharis","last_name":"Alvanos"},{"first_name":"Anika","full_name":"Hintze, Anika","last_name":"Hintze"},{"id":"3B8B25A8-F248-11E8-B48F-1D18A9856A87","first_name":"Peter","full_name":"Koppensteiner, Peter","last_name":"Koppensteiner","orcid":"0000-0002-3509-1948"},{"last_name":"Kleindienst","full_name":"Kleindienst, David","first_name":"David","id":"42E121A4-F248-11E8-B48F-1D18A9856A87"},{"id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","first_name":"Ryuichi","full_name":"Shigemoto, Ryuichi","last_name":"Shigemoto","orcid":"0000-0001-8761-9444"},{"first_name":"Carolin","last_name":"Wichmann","full_name":"Wichmann, Carolin"},{"last_name":"Moser","full_name":"Moser, Tobias","first_name":"Tobias"}],"publication_status":"published","citation":{"mla":"Butola, Tanvi, et al. “RIM-Binding Protein 2 Organizes Ca<sup>21</sup> Channel Topography and Regulates Release Probability and Vesicle Replenishment at a Fast Central Synapse.” <i>Journal of Neuroscience</i>, vol. 41, no. 37, Society for Neuroscience, 2021, pp. 7742–67, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.0586-21.2021\">10.1523/JNEUROSCI.0586-21.2021</a>.","ama":"Butola T, Alvanos T, Hintze A, et al. RIM-binding protein 2 organizes Ca<sup>21</sup> channel topography and regulates release probability and vesicle replenishment at a fast central synapse. <i>Journal of Neuroscience</i>. 2021;41(37):7742-7767. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.0586-21.2021\">10.1523/JNEUROSCI.0586-21.2021</a>","ista":"Butola T, Alvanos T, Hintze A, Koppensteiner P, Kleindienst D, Shigemoto R, Wichmann C, Moser T. 2021. RIM-binding protein 2 organizes Ca<sup>21</sup> channel topography and regulates release probability and vesicle replenishment at a fast central synapse. Journal of Neuroscience. 41(37), 7742–7767.","short":"T. Butola, T. Alvanos, A. Hintze, P. Koppensteiner, D. Kleindienst, R. Shigemoto, C. Wichmann, T. Moser, Journal of Neuroscience 41 (2021) 7742–7767.","ieee":"T. Butola <i>et al.</i>, “RIM-binding protein 2 organizes Ca<sup>21</sup> channel topography and regulates release probability and vesicle replenishment at a fast central synapse,” <i>Journal of Neuroscience</i>, vol. 41, no. 37. Society for Neuroscience, pp. 7742–7767, 2021.","apa":"Butola, T., Alvanos, T., Hintze, A., Koppensteiner, P., Kleindienst, D., Shigemoto, R., … Moser, T. (2021). RIM-binding protein 2 organizes Ca<sup>21</sup> channel topography and regulates release probability and vesicle replenishment at a fast central synapse. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.0586-21.2021\">https://doi.org/10.1523/JNEUROSCI.0586-21.2021</a>","chicago":"Butola, Tanvi, Theocharis Alvanos, Anika Hintze, Peter Koppensteiner, David Kleindienst, Ryuichi Shigemoto, Carolin Wichmann, and Tobias Moser. “RIM-Binding Protein 2 Organizes Ca<sup>21</sup> Channel Topography and Regulates Release Probability and Vesicle Replenishment at a Fast Central Synapse.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2021. <a href=\"https://doi.org/10.1523/JNEUROSCI.0586-21.2021\">https://doi.org/10.1523/JNEUROSCI.0586-21.2021</a>."},"_id":"10051","pmid":1,"publication_identifier":{"eissn":["1529-2401"],"issn":["0270-6474"]},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","acknowledgement":"This work was supported by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) through the Collaborative Sensory Research Center 1286 [to C.W. (A4) and T.M. (B5)] and under Germany’s Excellence Strategy Grant EXC 2067/1-390729940. We thank S. Gerke, A.J. Goldak, and C. Senger-Freitag for expert technical assistance; G. Hoch for developing image analysis routines; and S. Chepurwar and N. Strenzke for technical support and discussion regarding in vivo experiments. We also thank Dr. Christian Rosenmund, Dr. Katharina Grauel, and Dr. Stephan Sigrist for providing RIM-BP2 KO mice and Dr. Masahiko Watanabe for providing the anti-neurexin-antibody, and Dr. Toshihisa Ohtsuka for the anti-ELKS-antibody. J. Neef for help with the STED imaging and image analysis; E. Neher and S. Rizzoli for discussion and comments on the manuscript; K. Eguchi for help with the statistical analysis; and C. H. Huang and J. Neef for constant support and scientific discussion.","quality_controlled":"1","oa_version":"Published Version","oa":1,"volume":41,"date_updated":"2023-08-14T06:56:30Z","article_processing_charge":"No","publisher":"Society for Neuroscience","scopus_import":"1","language":[{"iso":"eng"}],"month":"09","article_type":"original","date_published":"2021-09-15T00:00:00Z","file":[{"date_updated":"2022-05-31T09:10:15Z","access_level":"open_access","date_created":"2022-05-31T09:10:15Z","checksum":"769ab627c7355a50ccfd445e43a5f351","file_name":"2021_JourNeuroscience_Butola.pdf","file_size":11571961,"file_id":"11423","creator":"dernst","content_type":"application/pdf","relation":"main_file","success":1}],"date_created":"2021-09-27T14:33:13Z","has_accepted_license":"1","department":[{"_id":"RySh"}],"intvolume":"        41","status":"public","day":"15","type":"journal_article","issue":"37","publication":"Journal of Neuroscience","file_date_updated":"2022-05-31T09:10:15Z","page":"7742-7767"},{"author":[{"id":"A057D288-3E88-11E9-986D-0CF4E5697425","first_name":"Fabrizio","orcid":"0000-0003-2623-5249","last_name":"Lombardi","full_name":"Lombardi, Fabrizio"},{"first_name":"Manuel","full_name":"Gómez-Extremera, Manuel","last_name":"Gómez-Extremera"},{"full_name":"Bernaola-Galván, Pedro","last_name":"Bernaola-Galván","first_name":"Pedro"},{"full_name":"Vetrivelan, Ramalingam","last_name":"Vetrivelan","first_name":"Ramalingam"},{"first_name":"Clifford B.","full_name":"Saper, Clifford B.","last_name":"Saper"},{"first_name":"Thomas E.","last_name":"Scammell","full_name":"Scammell, Thomas E."},{"last_name":"Ivanov","full_name":"Ivanov, Plamen Ch.","first_name":"Plamen Ch."}],"abstract":[{"text":"Origin and functions of intermittent transitions among sleep stages, including brief awakenings and arousals, constitute a challenge to the current homeostatic framework for sleep regulation, focusing on factors modulating sleep over large time scales. Here we propose that the complex micro-architecture characterizing sleep on scales of seconds and minutes results from intrinsic non-equilibrium critical dynamics. We investigate θ- and δ-wave dynamics in control rats and in rats where the sleep-promoting ventrolateral preoptic nucleus (VLPO) is lesioned (male Sprague-Dawley rats). We demonstrate that bursts in θ and δ cortical rhythms exhibit complex temporal organization, with long-range correlations and robust duality of power-law (θ-bursts, active phase) and exponential-like (δ-bursts, quiescent phase) duration distributions, features typical of non-equilibrium systems self-organizing at criticality. We show that such non-equilibrium behavior relates to anti-correlated coupling between θ- and δ-bursts, persists across a range of time scales, and is independent of the dominant physiologic state; indications of a basic principle in sleep regulation. Further, we find that VLPO lesions lead to a modulation of cortical dynamics resulting in altered dynamical parameters of θ- and δ-bursts and significant reduction in θ–δ coupling. Our empirical findings and model simulations demonstrate that θ–δ coupling is essential for the emerging non-equilibrium critical dynamics observed across the sleep–wake cycle, and indicate that VLPO neurons may have dual role for both sleep and arousal/brief wake activation. The uncovered critical behavior in sleep- and wake-related cortical rhythms indicates a mechanism essential for the micro-architecture of spontaneous sleep-stage and arousal transitions within a novel, non-homeostatic paradigm of sleep regulation.","lang":"eng"}],"citation":{"ieee":"F. Lombardi <i>et al.</i>, “Critical dynamics and coupling in bursts of cortical rhythms indicate non-homeostatic mechanism for sleep-stage transitions and dual role of VLPO neurons in both sleep and wake,” <i>Journal of Neuroscience</i>, vol. 40, no. 1. Society for Neuroscience, pp. 171–190, 2020.","apa":"Lombardi, F., Gómez-Extremera, M., Bernaola-Galván, P., Vetrivelan, R., Saper, C. B., Scammell, T. E., &#38; Ivanov, P. C. (2020). Critical dynamics and coupling in bursts of cortical rhythms indicate non-homeostatic mechanism for sleep-stage transitions and dual role of VLPO neurons in both sleep and wake. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/jneurosci.1278-19.2019\">https://doi.org/10.1523/jneurosci.1278-19.2019</a>","chicago":"Lombardi, Fabrizio, Manuel Gómez-Extremera, Pedro Bernaola-Galván, Ramalingam Vetrivelan, Clifford B. Saper, Thomas E. Scammell, and Plamen Ch. Ivanov. “Critical Dynamics and Coupling in Bursts of Cortical Rhythms Indicate Non-Homeostatic Mechanism for Sleep-Stage Transitions and Dual Role of VLPO Neurons in Both Sleep and Wake.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2020. <a href=\"https://doi.org/10.1523/jneurosci.1278-19.2019\">https://doi.org/10.1523/jneurosci.1278-19.2019</a>.","ama":"Lombardi F, Gómez-Extremera M, Bernaola-Galván P, et al. Critical dynamics and coupling in bursts of cortical rhythms indicate non-homeostatic mechanism for sleep-stage transitions and dual role of VLPO neurons in both sleep and wake. <i>Journal of Neuroscience</i>. 2020;40(1):171-190. doi:<a href=\"https://doi.org/10.1523/jneurosci.1278-19.2019\">10.1523/jneurosci.1278-19.2019</a>","mla":"Lombardi, Fabrizio, et al. “Critical Dynamics and Coupling in Bursts of Cortical Rhythms Indicate Non-Homeostatic Mechanism for Sleep-Stage Transitions and Dual Role of VLPO Neurons in Both Sleep and Wake.” <i>Journal of Neuroscience</i>, vol. 40, no. 1, Society for Neuroscience, 2020, pp. 171–90, doi:<a href=\"https://doi.org/10.1523/jneurosci.1278-19.2019\">10.1523/jneurosci.1278-19.2019</a>.","ista":"Lombardi F, Gómez-Extremera M, Bernaola-Galván P, Vetrivelan R, Saper CB, Scammell TE, Ivanov PC. 2020. Critical dynamics and coupling in bursts of cortical rhythms indicate non-homeostatic mechanism for sleep-stage transitions and dual role of VLPO neurons in both sleep and wake. Journal of Neuroscience. 40(1), 171–190.","short":"F. Lombardi, M. Gómez-Extremera, P. Bernaola-Galván, R. Vetrivelan, C.B. Saper, T.E. Scammell, P.C. Ivanov, Journal of Neuroscience 40 (2020) 171–190."},"publication_status":"published","oa_version":"Published Version","project":[{"grant_number":"754411","call_identifier":"H2020","name":"ISTplus - Postdoctoral Fellowships","_id":"260C2330-B435-11E9-9278-68D0E5697425"}],"quality_controlled":"1","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","publication_identifier":{"issn":["0270-6474"],"eissn":["1529-2401"]},"_id":"8084","pmid":1,"article_processing_charge":"No","volume":40,"oa":1,"date_updated":"2023-09-05T14:02:55Z","title":"Critical dynamics and coupling in bursts of cortical rhythms indicate non-homeostatic mechanism for sleep-stage transitions and dual role of VLPO neurons in both sleep and wake","external_id":{"pmid":["31694962"],"isi":["000505167600016"]},"ec_funded":1,"year":"2020","doi":"10.1523/jneurosci.1278-19.2019","ddc":["570"],"isi":1,"status":"public","intvolume":"        40","type":"journal_article","day":"02","page":"171-190","file_date_updated":"2020-07-22T11:44:48Z","publication":"Journal of Neuroscience","issue":"1","language":[{"iso":"eng"}],"scopus_import":"1","publisher":"Society for Neuroscience","article_type":"original","date_published":"2020-01-02T00:00:00Z","month":"01","file":[{"file_id":"8150","creator":"dernst","relation":"main_file","content_type":"application/pdf","success":1,"access_level":"open_access","date_updated":"2020-07-22T11:44:48Z","date_created":"2020-07-22T11:44:48Z","file_size":6646046,"file_name":"2020_JournNeuroscience_Lombardi.pdf"}],"date_created":"2020-07-05T15:24:51Z","department":[{"_id":"GaTk"}],"has_accepted_license":"1"},{"scopus_import":"1","publisher":"Society for Neuroscience","language":[{"iso":"eng"}],"month":"11","article_type":"original","date_published":"2014-11-19T00:00:00Z","date_created":"2018-12-11T11:55:14Z","file":[{"access_level":"open_access","date_updated":"2022-05-24T08:41:41Z","checksum":"6913e9bc26e9fc1c0441a739a4199229","date_created":"2022-05-24T08:41:41Z","file_size":3963728,"file_name":"2014_JournNeuroscience_Matsukawa.pdf","file_id":"11410","creator":"dernst","relation":"main_file","content_type":"application/pdf","success":1}],"has_accepted_license":"1","department":[{"_id":"RySh"}],"intvolume":"        34","status":"public","day":"19","type":"journal_article","publication":"Journal of Neuroscience","issue":"47","page":"15779 - 15792","file_date_updated":"2022-05-24T08:41:41Z","external_id":{"pmid":["25411505"]},"title":"Netrin-G/NGL complexes encode functional synaptic diversification","year":"2014","doi":"10.1523/JNEUROSCI.1141-14.2014","ddc":["570"],"abstract":[{"text":"Synaptic cell adhesion molecules are increasingly gaining attention for conferring specific properties to individual synapses. Netrin-G1 and netrin-G2 are trans-synaptic adhesion molecules that distribute on distinct axons, and their presence restricts the expression of their cognate receptors, NGL1 and NGL2, respectively, to specific subdendritic segments of target neurons. However, the neural circuits and functional roles of netrin-G isoform complexes remain unclear. Here, we use netrin-G-KO and NGL-KO mice to reveal that netrin-G1/NGL1 and netrin-G2/NGL2 interactions specify excitatory synapses in independent hippocampal pathways. In the hippocampal CA1 area, netrin-G1/NGL1 and netrin-G2/NGL2 were expressed in the temporoammonic and Schaffer collateral pathways, respectively. The lack of presynaptic netrin-Gs led to the dispersion of NGLs from postsynaptic membranes. In accord, netrin-G mutant synapses displayed opposing phenotypes in long-term and short-term plasticity through discrete biochemical pathways. The plasticity phenotypes in netrin-G-KOs were phenocopied in NGL-KOs, with a corresponding loss of netrin-Gs from presynaptic membranes. Our findings show that netrin-G/NGL interactions differentially control synaptic plasticity in distinct circuits via retrograde signaling mechanisms and explain how synaptic inputs are diversified to control neuronal activity.","lang":"eng"}],"author":[{"first_name":"Hiroshi","last_name":"Matsukawa","full_name":"Matsukawa, Hiroshi"},{"first_name":"Sachiko","last_name":"Akiyoshi Nishimura","full_name":"Akiyoshi Nishimura, Sachiko"},{"first_name":"Qi","full_name":"Zhang, Qi","last_name":"Zhang"},{"full_name":"Luján, Rafael","last_name":"Luján","first_name":"Rafael"},{"full_name":"Yamaguchi, Kazuhiko","last_name":"Yamaguchi","first_name":"Kazuhiko"},{"last_name":"Goto","full_name":"Goto, Hiromichi","first_name":"Hiromichi"},{"full_name":"Yaguchi, Kunio","last_name":"Yaguchi","first_name":"Kunio"},{"full_name":"Hashikawa, Tsutomu","last_name":"Hashikawa","first_name":"Tsutomu"},{"first_name":"Chie","last_name":"Sano","full_name":"Sano, Chie"},{"last_name":"Shigemoto","full_name":"Shigemoto, Ryuichi","orcid":"0000-0001-8761-9444","first_name":"Ryuichi","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Nakashiba, Toshiaki","last_name":"Nakashiba","first_name":"Toshiaki"},{"last_name":"Itohara","full_name":"Itohara, Shigeyoshi","first_name":"Shigeyoshi"}],"citation":{"chicago":"Matsukawa, Hiroshi, Sachiko Akiyoshi Nishimura, Qi Zhang, Rafael Luján, Kazuhiko Yamaguchi, Hiromichi Goto, Kunio Yaguchi, et al. “Netrin-G/NGL Complexes Encode Functional Synaptic Diversification.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2014. <a href=\"https://doi.org/10.1523/JNEUROSCI.1141-14.2014\">https://doi.org/10.1523/JNEUROSCI.1141-14.2014</a>.","ieee":"H. Matsukawa <i>et al.</i>, “Netrin-G/NGL complexes encode functional synaptic diversification,” <i>Journal of Neuroscience</i>, vol. 34, no. 47. Society for Neuroscience, pp. 15779–15792, 2014.","apa":"Matsukawa, H., Akiyoshi Nishimura, S., Zhang, Q., Luján, R., Yamaguchi, K., Goto, H., … Itohara, S. (2014). Netrin-G/NGL complexes encode functional synaptic diversification. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.1141-14.2014\">https://doi.org/10.1523/JNEUROSCI.1141-14.2014</a>","short":"H. Matsukawa, S. Akiyoshi Nishimura, Q. Zhang, R. Luján, K. Yamaguchi, H. Goto, K. Yaguchi, T. Hashikawa, C. Sano, R. Shigemoto, T. Nakashiba, S. Itohara, Journal of Neuroscience 34 (2014) 15779–15792.","ista":"Matsukawa H, Akiyoshi Nishimura S, Zhang Q, Luján R, Yamaguchi K, Goto H, Yaguchi K, Hashikawa T, Sano C, Shigemoto R, Nakashiba T, Itohara S. 2014. Netrin-G/NGL complexes encode functional synaptic diversification. Journal of Neuroscience. 34(47), 15779–15792.","ama":"Matsukawa H, Akiyoshi Nishimura S, Zhang Q, et al. Netrin-G/NGL complexes encode functional synaptic diversification. <i>Journal of Neuroscience</i>. 2014;34(47):15779-15792. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.1141-14.2014\">10.1523/JNEUROSCI.1141-14.2014</a>","mla":"Matsukawa, Hiroshi, et al. “Netrin-G/NGL Complexes Encode Functional Synaptic Diversification.” <i>Journal of Neuroscience</i>, vol. 34, no. 47, Society for Neuroscience, 2014, pp. 15779–92, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.1141-14.2014\">10.1523/JNEUROSCI.1141-14.2014</a>."},"publication_status":"published","publication_identifier":{"eissn":["1529-2401"],"issn":["0270-6474"]},"pmid":1,"_id":"2018","oa_version":"Published Version","quality_controlled":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","acknowledgement":"This work was supported by “Funding Program for World-Leading Innovative R&D on Science and Technology (FIRST Program)” initiated by the Council for Science and Technology Policy.","article_processing_charge":"No","date_updated":"2022-05-24T08:54:54Z","publist_id":"5054","volume":34,"oa":1},{"year":"2014","doi":"10.1523/jneurosci.5368-13.2014","external_id":{"pmid":["25505325"]},"title":"GLOBIN-5-dependent O2 responses are regulated by PDL-1/PrBP that targets prenylated soluble guanylate cyclases to dendritic endings","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"ddc":["570"],"publication_status":"published","citation":{"ista":"Gross E, Soltesz Z, Oda S, Zelmanovich V, Abergel Z, de Bono M. 2014. GLOBIN-5-dependent O2 responses are regulated by PDL-1/PrBP that targets prenylated soluble guanylate cyclases to dendritic endings. Journal of Neuroscience. 34(50), 16726–16738.","short":"E. Gross, Z. Soltesz, S. Oda, V. Zelmanovich, Z. Abergel, M. de Bono, Journal of Neuroscience 34 (2014) 16726–16738.","ama":"Gross E, Soltesz Z, Oda S, Zelmanovich V, Abergel Z, de Bono M. GLOBIN-5-dependent O2 responses are regulated by PDL-1/PrBP that targets prenylated soluble guanylate cyclases to dendritic endings. <i>Journal of Neuroscience</i>. 2014;34(50):16726-16738. doi:<a href=\"https://doi.org/10.1523/jneurosci.5368-13.2014\">10.1523/jneurosci.5368-13.2014</a>","mla":"Gross, E., et al. “GLOBIN-5-Dependent O2 Responses Are Regulated by PDL-1/PrBP That Targets Prenylated Soluble Guanylate Cyclases to Dendritic Endings.” <i>Journal of Neuroscience</i>, vol. 34, no. 50, Society for Neuroscience, 2014, pp. 16726–38, doi:<a href=\"https://doi.org/10.1523/jneurosci.5368-13.2014\">10.1523/jneurosci.5368-13.2014</a>.","chicago":"Gross, E., Z. Soltesz, S. Oda, V. Zelmanovich, Z. Abergel, and Mario de Bono. “GLOBIN-5-Dependent O2 Responses Are Regulated by PDL-1/PrBP That Targets Prenylated Soluble Guanylate Cyclases to Dendritic Endings.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2014. <a href=\"https://doi.org/10.1523/jneurosci.5368-13.2014\">https://doi.org/10.1523/jneurosci.5368-13.2014</a>.","apa":"Gross, E., Soltesz, Z., Oda, S., Zelmanovich, V., Abergel, Z., &#38; de Bono, M. (2014). GLOBIN-5-dependent O2 responses are regulated by PDL-1/PrBP that targets prenylated soluble guanylate cyclases to dendritic endings. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/jneurosci.5368-13.2014\">https://doi.org/10.1523/jneurosci.5368-13.2014</a>","ieee":"E. Gross, Z. Soltesz, S. Oda, V. Zelmanovich, Z. Abergel, and M. de Bono, “GLOBIN-5-dependent O2 responses are regulated by PDL-1/PrBP that targets prenylated soluble guanylate cyclases to dendritic endings,” <i>Journal of Neuroscience</i>, vol. 34, no. 50. Society for Neuroscience, pp. 16726–16738, 2014."},"abstract":[{"text":"Aerobic animals constantly monitor and adapt to changes in O2 levels. The molecular mechanisms involved in sensing O2 are, however, incompletely understood. Previous studies showed that a hexacoordinated globin called GLB-5 tunes the dynamic range of O2-sensing neurons in natural C. elegans isolates, but is defective in the N2 lab reference strain (McGrath et al., 2009; Persson et al., 2009). GLB-5 enables a sharp behavioral switch when O2 changes between 21 and 17%. Here, we show that GLB-5 also confers rapid behavioral and cellular recovery from exposure to hypoxia. Hypoxia reconfigures O2-evoked Ca2+ responses in the URX O2 sensors, and GLB-5 enables rapid recovery of these responses upon re-oxygenation. Forward genetic screens indicate that GLB-5's effects on O2 sensing require PDL-1, the C. elegans ortholog of mammalian PrBP/PDE6δ protein. In mammals, PDE6δ regulates the traffic and activity of prenylated proteins (Zhang et al., 2004; Norton et al., 2005). PDL-1 promotes localization of GCY-33 and GCY-35, atypical soluble guanylate cyclases that act as O2 sensors, to the dendritic endings of URX and BAG neurons, where they colocalize with GLB-5. Both GCY-33 and GCY-35 are predicted to be prenylated. Dendritic localization is not essential for GCY-35 to function as an O2 sensor, but disrupting pdl-1 alters the URX neuron's O2 response properties. Functional GLB-5 can restore dendritic localization of GCY-33 in pdl-1 mutants, suggesting GCY-33 and GLB-5 are in a complex. Our data suggest GLB-5 and the soluble guanylate cyclases operate in close proximity to sculpt O2 responses.","lang":"eng"}],"author":[{"full_name":"Gross, E.","last_name":"Gross","first_name":"E."},{"first_name":"Z.","full_name":"Soltesz, Z.","last_name":"Soltesz"},{"last_name":"Oda","full_name":"Oda, S.","first_name":"S."},{"first_name":"V.","full_name":"Zelmanovich, V.","last_name":"Zelmanovich"},{"first_name":"Z.","full_name":"Abergel, Z.","last_name":"Abergel"},{"id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8347-0443","last_name":"de Bono","full_name":"de Bono, Mario","first_name":"Mario"}],"oa":1,"volume":34,"date_updated":"2021-01-12T08:06:14Z","_id":"6126","pmid":1,"extern":"1","publication_identifier":{"issn":["0270-6474","1529-2401"]},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","quality_controlled":"1","oa_version":"Published Version","month":"12","date_published":"2014-12-10T00:00:00Z","publisher":"Society for Neuroscience","language":[{"iso":"eng"}],"has_accepted_license":"1","file":[{"creator":"kschuh","file_id":"6127","content_type":"application/pdf","relation":"main_file","date_created":"2019-03-19T14:55:58Z","checksum":"a3dd71969f94c43909327cd083283d4b","file_name":"2014_SFN_Gross.pdf","file_size":3263422,"date_updated":"2020-07-14T12:47:20Z","access_level":"open_access"}],"date_created":"2019-03-19T14:52:26Z","day":"10","type":"journal_article","intvolume":"        34","status":"public","issue":"50","publication":"Journal of Neuroscience","file_date_updated":"2020-07-14T12:47:20Z","page":"16726-16738"},{"user_id":"D865714E-FA4E-11E9-B85B-F5C5E5697425","oa_version":"Published Version","quality_controlled":"1","pmid":1,"_id":"8025","publication_identifier":{"issn":["0270-6474","1529-2401"]},"extern":"1","oa":1,"date_updated":"2021-01-12T08:16:36Z","volume":31,"article_processing_charge":"No","author":[{"last_name":"Woodruff","full_name":"Woodruff, A. R.","first_name":"A. R."},{"last_name":"McGarry","full_name":"McGarry, L. M.","first_name":"L. M."},{"id":"CB6FF8D2-008F-11EA-8E08-2637E6697425","first_name":"Tim P","orcid":"0000-0003-3295-6181","full_name":"Vogels, Tim P","last_name":"Vogels"},{"last_name":"Inan","full_name":"Inan, M.","first_name":"M."},{"first_name":"S. A.","last_name":"Anderson","full_name":"Anderson, S. A."},{"last_name":"Yuste","full_name":"Yuste, R.","first_name":"R."}],"abstract":[{"text":"Chandelier (axoaxonic) cells (ChCs) are a distinct group of GABAergic interneurons that innervate the axon initial segments of pyramidal cells. However, their circuit role and the function of their clearly defined anatomical specificity remain unclear. Recent work has demonstrated that chandelier cells can produce depolarizing GABAergic PSPs, occasionally driving postsynaptic targets to spike. On the other hand, other work suggests that ChCs are hyperpolarizing and may have an inhibitory role. These disparate functional effects may reflect heterogeneity among ChCs. Here, using brain slices from transgenic mouse strains, we first demonstrate that, across different neocortical areas and genetic backgrounds, upper Layer 2/3 ChCs belong to a single electrophysiologically and morphologically defined population, extensively sampling Layer 1 inputs with asymmetric dendrites. Consistent with being a single cell type, we find electrical coupling between ChCs. We then investigate the effect of chandelier cell activation on pyramidal neuron spiking in several conditions, ranging from the resting membrane potential to stimuli designed to approximate in vivo membrane potential dynamics. We find that under quiescent conditions, chandelier cells are capable of both promoting and inhibiting spike generation, depending on the postsynaptic membrane potential. However, during in vivo-like membrane potential fluctuations, the dominant postsynaptic effect was a strong inhibition. Thus, neocortical chandelier cells, even from within a homogeneous population, appear to play a dual role in the circuit, helping to activate quiescent pyramidal neurons, while at the same time inhibiting active ones.","lang":"eng"}],"publication_status":"published","citation":{"mla":"Woodruff, A. R., et al. “State-Dependent Function of Neocortical Chandelier Cells.” <i>Journal of Neuroscience</i>, vol. 31, no. 49, Society for Neuroscience, 2011, pp. 17872–86, doi:<a href=\"https://doi.org/10.1523/jneurosci.3894-11.2011\">10.1523/jneurosci.3894-11.2011</a>.","ama":"Woodruff AR, McGarry LM, Vogels TP, Inan M, Anderson SA, Yuste R. State-dependent function of neocortical chandelier cells. <i>Journal of Neuroscience</i>. 2011;31(49):17872-17886. doi:<a href=\"https://doi.org/10.1523/jneurosci.3894-11.2011\">10.1523/jneurosci.3894-11.2011</a>","ista":"Woodruff AR, McGarry LM, Vogels TP, Inan M, Anderson SA, Yuste R. 2011. State-dependent function of neocortical chandelier cells. Journal of Neuroscience. 31(49), 17872–17886.","short":"A.R. Woodruff, L.M. McGarry, T.P. Vogels, M. Inan, S.A. Anderson, R. Yuste, Journal of Neuroscience 31 (2011) 17872–17886.","apa":"Woodruff, A. R., McGarry, L. M., Vogels, T. P., Inan, M., Anderson, S. A., &#38; Yuste, R. (2011). State-dependent function of neocortical chandelier cells. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/jneurosci.3894-11.2011\">https://doi.org/10.1523/jneurosci.3894-11.2011</a>","ieee":"A. R. Woodruff, L. M. McGarry, T. P. Vogels, M. Inan, S. A. Anderson, and R. Yuste, “State-dependent function of neocortical chandelier cells,” <i>Journal of Neuroscience</i>, vol. 31, no. 49. Society for Neuroscience, pp. 17872–17886, 2011.","chicago":"Woodruff, A. R., L. M. McGarry, Tim P Vogels, M. Inan, S. A. Anderson, and R. Yuste. “State-Dependent Function of Neocortical Chandelier Cells.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2011. <a href=\"https://doi.org/10.1523/jneurosci.3894-11.2011\">https://doi.org/10.1523/jneurosci.3894-11.2011</a>."},"main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4071969/"}],"external_id":{"pmid":["22159102"]},"title":"State-dependent function of neocortical chandelier cells","doi":"10.1523/jneurosci.3894-11.2011","year":"2011","page":"17872-17886","issue":"49","publication":"Journal of Neuroscience","status":"public","intvolume":"        31","type":"journal_article","day":"7","date_created":"2020-06-25T13:09:49Z","language":[{"iso":"eng"}],"publisher":"Society for Neuroscience","article_type":"original","date_published":"2011-12-07T00:00:00Z","month":"12"},{"type":"journal_article","day":"16","status":"public","intvolume":"        25","page":"10786-10795","issue":"46","publication":"Journal of Neuroscience","date_published":"2005-11-16T00:00:00Z","article_type":"original","month":"11","language":[{"iso":"eng"}],"publisher":"Society for Neuroscience","date_created":"2020-06-25T13:12:33Z","publication_status":"published","citation":{"ista":"Vogels TP, Abbott LF. 2005. Signal propagation and logic gating in networks of integrate-and-fire neurons. Journal of Neuroscience. 25(46), 10786–10795.","short":"T.P. Vogels, L.F. Abbott, Journal of Neuroscience 25 (2005) 10786–10795.","ama":"Vogels TP, Abbott LF. Signal propagation and logic gating in networks of integrate-and-fire neurons. <i>Journal of Neuroscience</i>. 2005;25(46):10786-10795. doi:<a href=\"https://doi.org/10.1523/jneurosci.3508-05.2005\">10.1523/jneurosci.3508-05.2005</a>","mla":"Vogels, Tim P., and L. F. Abbott. “Signal Propagation and Logic Gating in Networks of Integrate-and-Fire Neurons.” <i>Journal of Neuroscience</i>, vol. 25, no. 46, Society for Neuroscience, 2005, pp. 10786–95, doi:<a href=\"https://doi.org/10.1523/jneurosci.3508-05.2005\">10.1523/jneurosci.3508-05.2005</a>.","chicago":"Vogels, Tim P, and L. F. Abbott. “Signal Propagation and Logic Gating in Networks of Integrate-and-Fire Neurons.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2005. <a href=\"https://doi.org/10.1523/jneurosci.3508-05.2005\">https://doi.org/10.1523/jneurosci.3508-05.2005</a>.","ieee":"T. P. Vogels and L. F. Abbott, “Signal propagation and logic gating in networks of integrate-and-fire neurons,” <i>Journal of Neuroscience</i>, vol. 25, no. 46. Society for Neuroscience, pp. 10786–10795, 2005.","apa":"Vogels, T. P., &#38; Abbott, L. F. (2005). Signal propagation and logic gating in networks of integrate-and-fire neurons. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/jneurosci.3508-05.2005\">https://doi.org/10.1523/jneurosci.3508-05.2005</a>"},"author":[{"id":"CB6FF8D2-008F-11EA-8E08-2637E6697425","orcid":"0000-0003-3295-6181","full_name":"Vogels, Tim P","last_name":"Vogels","first_name":"Tim P"},{"last_name":"Abbott","full_name":"Abbott, L. F.","first_name":"L. F."}],"abstract":[{"lang":"eng","text":"Transmission of signals within the brain is essential for cognitive function, but it is not clear how neural circuits support reliable and accurate signal propagation over a sufficiently large dynamic range. Two modes of propagation have been studied: synfire chains, in which synchronous activity travels through feedforward layers of a neuronal network, and the propagation of fluctuations in firing rate across these layers. In both cases, a sufficient amount of noise, which was added to previous models from an external source, had to be included to support stable propagation. Sparse, randomly connected networks of spiking model neurons can generate chaotic patterns of activity. We investigate whether this activity, which is a more realistic noise source, is sufficient to allow for signal transmission. We find that, for rate-coded signals but not for synfire chains, such networks support robust and accurate signal reproduction through up to six layers if appropriate adjustments are made in synaptic strengths. We investigate the factors affecting transmission and show that multiple signals can propagate simultaneously along different pathways. Using this feature, we show how different types of logic gates can arise within the architecture of the random network through the strengthening of specific synapses."}],"date_updated":"2021-01-12T08:16:37Z","volume":25,"oa":1,"article_processing_charge":"No","user_id":"D865714E-FA4E-11E9-B85B-F5C5E5697425","oa_version":"Published Version","quality_controlled":"1","pmid":1,"_id":"8028","extern":"1","publication_identifier":{"issn":["0270-6474","1529-2401"]},"year":"2005","doi":"10.1523/jneurosci.3508-05.2005","external_id":{"pmid":["16291952"]},"title":"Signal propagation and logic gating in networks of integrate-and-fire neurons","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6725859/"}]},{"abstract":[{"text":"In this investigation, we report identification and characterization of a 95 kDa postsynaptic density protein (PSD-95)/discs-large/ ZO-1 (PDZ) domain-containing protein termed tamalin, also recently named GRP1-associated scaffold protein (GRASP), that interacts with group 1 metabotropic glutamate receptors (mGluRs). The yeast two-hybrid system and in vitro pull-down assays indicated that the PDZ domain-containing, amino-terminal half of tamalin directly binds to the class I PDZ-binding motif of group 1 mGluRs. The C-terminal half of tamalin also bound to cytohesins, the members of guanine nucleotide exchange factors (GEFs) specific for the ADP-ribosylation factor (ARF) family of small GTP-binding proteins. Tamalin mRNA is expressed predominantly in the telencephalic region and highly overlaps with the expression of group 1 mGluR mRNAs. Both tamalin and cytohesin-2 were enriched and codistributed with mGluR1a in postsynaptic membrane fractions. Importantly, recombinant and native mGluR1a/tamalin/cytohesin-2 complexes were coimmunoprecipitated from transfected COS-7 cells and rat brain tissue, respectively. Transfection of tamalin and mutant tamalin lacking a cytohesin-binding domain caused an increase and decrease in cell-surface expression of mGluR1a in COS-7 cells, respectively. Furthermore, adenovirus-mediated expression of tamalin and dominant-negative tamalin facilitated and reduced the neuritic distribution of endogenous mGluR5 in cultured hippocampal neurons, respectively. The results indicate that tamalin plays a key role in the association of group 1 mGluRs with the ARF-specific GEF proteins and contributes to intracellular trafficking and the macromolecular organization of group 1 mGluRs at synapses.","lang":"eng"}],"author":[{"first_name":"Jun","full_name":"Kitano, Jun","last_name":"Kitano"},{"last_name":"Kimura","full_name":"Kimura, Kouji","first_name":"Kouji"},{"first_name":"Yoshimitsu","last_name":"Yamazaki","full_name":"Yamazaki, Yoshimitsu"},{"first_name":"Takeshi","full_name":"Soda, Takeshi","last_name":"Soda"},{"first_name":"Ryuichi","full_name":"Shigemoto, Ryuichi","last_name":"Shigemoto","orcid":"0000-0001-8761-9444","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Yoshiaki","last_name":"Nakajima","full_name":"Nakajima, Yoshiaki"},{"first_name":"Shigetada","full_name":"Nakanishi, Shigetada","last_name":"Nakanishi"}],"citation":{"mla":"Kitano, Jun, et al. “Tamalin, a PDZ Domain-Containing Protein, Links a Protein Complex Formation of Group 1 Metabotropic Glutamate Receptors and the Guanine Nucleotide Exchange Factor Cytohesins.” <i>Journal of Neuroscience</i>, vol. 22, no. 4, Society for Neuroscience, 2002, pp. 1280–89, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.22-04-01280.2002\">10.1523/JNEUROSCI.22-04-01280.2002</a>.","ama":"Kitano J, Kimura K, Yamazaki Y, et al. Tamalin, a PDZ domain-containing protein, links a protein complex formation of group 1 metabotropic glutamate receptors and the guanine nucleotide exchange factor cytohesins. <i>Journal of Neuroscience</i>. 2002;22(4):1280-1289. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.22-04-01280.2002\">10.1523/JNEUROSCI.22-04-01280.2002</a>","short":"J. Kitano, K. Kimura, Y. Yamazaki, T. Soda, R. Shigemoto, Y. Nakajima, S. Nakanishi, Journal of Neuroscience 22 (2002) 1280–1289.","ista":"Kitano J, Kimura K, Yamazaki Y, Soda T, Shigemoto R, Nakajima Y, Nakanishi S. 2002. Tamalin, a PDZ domain-containing protein, links a protein complex formation of group 1 metabotropic glutamate receptors and the guanine nucleotide exchange factor cytohesins. Journal of Neuroscience. 22(4), 1280–1289.","ieee":"J. Kitano <i>et al.</i>, “Tamalin, a PDZ domain-containing protein, links a protein complex formation of group 1 metabotropic glutamate receptors and the guanine nucleotide exchange factor cytohesins,” <i>Journal of Neuroscience</i>, vol. 22, no. 4. Society for Neuroscience, pp. 1280–1289, 2002.","apa":"Kitano, J., Kimura, K., Yamazaki, Y., Soda, T., Shigemoto, R., Nakajima, Y., &#38; Nakanishi, S. (2002). Tamalin, a PDZ domain-containing protein, links a protein complex formation of group 1 metabotropic glutamate receptors and the guanine nucleotide exchange factor cytohesins. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.22-04-01280.2002\">https://doi.org/10.1523/JNEUROSCI.22-04-01280.2002</a>","chicago":"Kitano, Jun, Kouji Kimura, Yoshimitsu Yamazaki, Takeshi Soda, Ryuichi Shigemoto, Yoshiaki Nakajima, and Shigetada Nakanishi. “Tamalin, a PDZ Domain-Containing Protein, Links a Protein Complex Formation of Group 1 Metabotropic Glutamate Receptors and the Guanine Nucleotide Exchange Factor Cytohesins.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2002. <a href=\"https://doi.org/10.1523/JNEUROSCI.22-04-01280.2002\">https://doi.org/10.1523/JNEUROSCI.22-04-01280.2002</a>."},"publication_status":"published","extern":"1","publication_identifier":{"issn":["0270-6474"]},"pmid":1,"_id":"2613","quality_controlled":"1","oa_version":"None","acknowledgement":"This work was supported in part by research grants from the Ministry of Education, Science and Culture of Japan. We thank Bert Vogelstein for providing adenoviral recombination vectors and Haruhiko Bito for a gift of the enolase promoter and technical advice. We are grateful to Atsushi Nishimune and Satoshi Kaneko for technical advice and Kumlesh K. Dev for careful reading of this manuscript.","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","article_processing_charge":"No","publist_id":"4285","date_updated":"2023-07-25T11:34:46Z","volume":22,"external_id":{"pmid":["11850456"]},"title":"Tamalin, a PDZ domain-containing protein, links a protein complex formation of group 1 metabotropic glutamate receptors and the guanine nucleotide exchange factor cytohesins","doi":"10.1523/JNEUROSCI.22-04-01280.2002","year":"2002","intvolume":"        22","status":"public","day":"15","type":"journal_article","publication":"Journal of Neuroscience","issue":"4","page":"1280 - 1289","scopus_import":"1","publisher":"Society for Neuroscience","language":[{"iso":"eng"}],"month":"02","date_published":"2002-02-15T00:00:00Z","article_type":"original","date_created":"2018-12-11T11:58:40Z"},{"date_created":"2018-12-11T12:05:15Z","scopus_import":"1","publisher":"Society for Neuroscience","language":[{"iso":"eng"}],"month":"12","article_type":"original","date_published":"2002-12-01T00:00:00Z","publication":"Journal of Neuroscience","issue":"24","page":"10593 - 10602","intvolume":"        22","status":"public","day":"01","type":"journal_article","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6758411/","open_access":"1"}],"title":"Timing and efficacy of Ca(2+) channel activation in hippocampal mossy fiber boutons","external_id":{"pmid":["12486151"]},"doi":"10.1523/JNEUROSCI.22-24-10593.2002","year":"2002","publication_identifier":{"issn":["0270-6474"]},"extern":"1","pmid":1,"_id":"3802","quality_controlled":"1","oa_version":"Published Version","acknowledgement":"J.B. was supported by grants from the Deutsche Forschungsgemeinschaft (Bi 642/1-2 and SFB 505/C9). We thank Dr. U. Kraushaar, Dr. S. Hefft, and C. Schmidt-Hieber for critically reading this manuscript, F. Heyde for secretarial help, and A. Blomenkamp and K. Winterhalter for technical assistance.","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","article_processing_charge":"No","date_updated":"2023-06-13T13:19:45Z","oa":1,"volume":22,"publist_id":"2407","abstract":[{"lang":"eng","text":"The presynaptic Ca2+ signal is a key determinant of transmitter release at chemical synapses. In cortical synaptic terminals, however, little is known about the kinetic properties of the presynaptic Ca2+ channels. To investigate the timing and magnitude of the presynaptic Ca2+ inflow, we performed whole-cell patch-clamp recordings from mossy fiber boutons (MFBs) in rat hippocampus. MFBs showed large high-voltage-activated Ca(2+) currents, with a maximal amplitude of approximately 100 pA at a membrane potential of 0 mV. Both activation and deactivation were fast, with time constants in the submillisecond range at a temperature of approximately 23 degrees C. An MFB action potential (AP) applied as a voltage-clamp command evoked a transient Ca2+ current with an average amplitude of approximately 170 pA and a half-duration of 580 microsec. A prepulse to +40 mV had only minimal effects on the AP-evoked Ca2+ current, indicating that presynaptic APs open the voltage-gated Ca2+ channels very effectively. On the basis of the experimental data, we developed a kinetic model with four closed states and one open state, linked by voltage-dependent rate constants. Simulations of the Ca2+ current could reproduce the experimental data, including the large amplitude and rapid time course of the current evoked by MFB APs. Furthermore, the simulations indicate that the shape of the presynaptic AP and the gating kinetics of the Ca2+ channels are tuned to produce a maximal Ca2+ influx during a minimal period of time. The precise timing and high efficacy of Ca2+ channel activation at this cortical glutamatergic synapse may be important for synchronous transmitter release and temporal information processing."}],"author":[{"first_name":"Josef","last_name":"Bischofberger","full_name":"Bischofberger, Josef"},{"last_name":"Geiger","full_name":"Geiger, Jörg","first_name":"Jörg"},{"first_name":"Peter M","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"}],"citation":{"apa":"Bischofberger, J., Geiger, J., &#38; Jonas, P. M. (2002). Timing and efficacy of Ca(2+) channel activation in hippocampal mossy fiber boutons. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.22-24-10593.2002\">https://doi.org/10.1523/JNEUROSCI.22-24-10593.2002</a>","ieee":"J. Bischofberger, J. Geiger, and P. M. Jonas, “Timing and efficacy of Ca(2+) channel activation in hippocampal mossy fiber boutons,” <i>Journal of Neuroscience</i>, vol. 22, no. 24. Society for Neuroscience, pp. 10593–10602, 2002.","chicago":"Bischofberger, Josef, Jörg Geiger, and Peter M Jonas. “Timing and Efficacy of Ca(2+) Channel Activation in Hippocampal Mossy Fiber Boutons.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2002. <a href=\"https://doi.org/10.1523/JNEUROSCI.22-24-10593.2002\">https://doi.org/10.1523/JNEUROSCI.22-24-10593.2002</a>.","mla":"Bischofberger, Josef, et al. “Timing and Efficacy of Ca(2+) Channel Activation in Hippocampal Mossy Fiber Boutons.” <i>Journal of Neuroscience</i>, vol. 22, no. 24, Society for Neuroscience, 2002, pp. 10593–602, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.22-24-10593.2002\">10.1523/JNEUROSCI.22-24-10593.2002</a>.","ama":"Bischofberger J, Geiger J, Jonas PM. Timing and efficacy of Ca(2+) channel activation in hippocampal mossy fiber boutons. <i>Journal of Neuroscience</i>. 2002;22(24):10593-10602. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.22-24-10593.2002\">10.1523/JNEUROSCI.22-24-10593.2002</a>","ista":"Bischofberger J, Geiger J, Jonas PM. 2002. Timing and efficacy of Ca(2+) channel activation in hippocampal mossy fiber boutons. Journal of Neuroscience. 22(24), 10593–10602.","short":"J. Bischofberger, J. Geiger, P.M. Jonas, Journal of Neuroscience 22 (2002) 10593–10602."},"publication_status":"published"},{"oa":1,"date_updated":"2023-05-24T08:47:53Z","publist_id":"4288","volume":21,"article_processing_charge":"No","acknowledgement":"This work was supported in part by the Biotechnology and Biological Sciences Research Council and Medical Research Council (UK). We thank Doris Ruegg for sequencing, Gemma Texido and Klaus Rajewsky for pTV-0 DNA, J.-F. Pin for mGluR8 cDNA, K. von Figura for E14 ES cells, Pedro Grandes for histological examination of brain sections, Christoph Wiessner for help with plots and statistics, Valerie Schuler for help with Western blots, and the team of the Novartis special strain breeding facility for their support.","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","quality_controlled":"1","oa_version":"Published Version","pmid":1,"_id":"2610","publication_identifier":{"issn":["0270-6474"]},"extern":"1","publication_status":"published","citation":{"ama":"Sansig G, Bushell T, Clarke V, et al. Increased seizure susceptibility in mice lacking metabotropic glutamate receptor 7. <i>Journal of Neuroscience</i>. 2001;21(22):8734-8745. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.21-22-08734.2001\">10.1523/JNEUROSCI.21-22-08734.2001</a>","mla":"Sansig, Gilles, et al. “Increased Seizure Susceptibility in Mice Lacking Metabotropic Glutamate Receptor 7.” <i>Journal of Neuroscience</i>, vol. 21, no. 22, Society for Neuroscience, 2001, pp. 8734–45, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.21-22-08734.2001\">10.1523/JNEUROSCI.21-22-08734.2001</a>.","ista":"Sansig G, Bushell T, Clarke V, Rozov A, Burnashev N, Portet C, Gasparini F, Schmutz M, Klebs K, Shigemoto R, Flor P, Kühn R, Knoepfel T, Schroeder M, Hampson D, Collett V, Zhang C, Duvoisin R, Collingridge G, Van Der Putten H. 2001. Increased seizure susceptibility in mice lacking metabotropic glutamate receptor 7. Journal of Neuroscience. 21(22), 8734–8745.","short":"G. Sansig, T. Bushell, V. Clarke, A. Rozov, N. Burnashev, C. Portet, F. Gasparini, M. Schmutz, K. Klebs, R. Shigemoto, P. Flor, R. Kühn, T. Knoepfel, M. Schroeder, D. Hampson, V. Collett, C. Zhang, R. Duvoisin, G. Collingridge, H. Van Der Putten, Journal of Neuroscience 21 (2001) 8734–8745.","apa":"Sansig, G., Bushell, T., Clarke, V., Rozov, A., Burnashev, N., Portet, C., … Van Der Putten, H. (2001). Increased seizure susceptibility in mice lacking metabotropic glutamate receptor 7. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.21-22-08734.2001\">https://doi.org/10.1523/JNEUROSCI.21-22-08734.2001</a>","ieee":"G. Sansig <i>et al.</i>, “Increased seizure susceptibility in mice lacking metabotropic glutamate receptor 7,” <i>Journal of Neuroscience</i>, vol. 21, no. 22. Society for Neuroscience, pp. 8734–8745, 2001.","chicago":"Sansig, Gilles, Trevor Bushell, Vernon Clarke, Andrei Rozov, Nail Burnashev, Chantal Portet, Fabrizio Gasparini, et al. “Increased Seizure Susceptibility in Mice Lacking Metabotropic Glutamate Receptor 7.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2001. <a href=\"https://doi.org/10.1523/JNEUROSCI.21-22-08734.2001\">https://doi.org/10.1523/JNEUROSCI.21-22-08734.2001</a>."},"author":[{"first_name":"Gilles","full_name":"Sansig, Gilles","last_name":"Sansig"},{"full_name":"Bushell, Trevor","last_name":"Bushell","first_name":"Trevor"},{"first_name":"Vernon","full_name":"Clarke, Vernon","last_name":"Clarke"},{"full_name":"Rozov, Andrei","last_name":"Rozov","first_name":"Andrei"},{"full_name":"Burnashev, Nail","last_name":"Burnashev","first_name":"Nail"},{"first_name":"Chantal","last_name":"Portet","full_name":"Portet, Chantal"},{"first_name":"Fabrizio","full_name":"Gasparini, Fabrizio","last_name":"Gasparini"},{"full_name":"Schmutz, Markus","last_name":"Schmutz","first_name":"Markus"},{"first_name":"Klaus","last_name":"Klebs","full_name":"Klebs, Klaus"},{"id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8761-9444","last_name":"Shigemoto","full_name":"Shigemoto, Ryuichi","first_name":"Ryuichi"},{"first_name":"Peter","last_name":"Flor","full_name":"Flor, Peter"},{"last_name":"Kühn","full_name":"Kühn, Rainer","first_name":"Rainer"},{"full_name":"Knoepfel, Thomas","last_name":"Knoepfel","first_name":"Thomas"},{"first_name":"Markus","last_name":"Schroeder","full_name":"Schroeder, Markus"},{"first_name":"David","last_name":"Hampson","full_name":"Hampson, David"},{"last_name":"Collett","full_name":"Collett, Valerie","first_name":"Valerie"},{"last_name":"Zhang","full_name":"Zhang, Congxiao","first_name":"Congxiao"},{"full_name":"Duvoisin, Robert","last_name":"Duvoisin","first_name":"Robert"},{"last_name":"Collingridge","full_name":"Collingridge, Graham","first_name":"Graham"},{"last_name":"Van Der Putten","full_name":"Van Der Putten, Herman","first_name":"Herman"}],"abstract":[{"lang":"eng","text":"To study the role of mGlu7 receptors (mGluR7), we used homologous recombination to generate mice lacking this metabotropic receptor subtype (mGluR7 -/-). After the serendipitous discovery of a sensory stimulus-evoked epileptic phenotype, we tested two convulsant drugs, pentylenetetrazole (PTZ) and bicuculline. In animals aged 12 weeks and older, subthreshold doses of these drugs induced seizures in mGluR7 -/-, but not in mGluR7 +/-, mice. PTZ-induced seizures were inhibited by three standard anticonvulsant drugs, but not by the group III selective mGluR agonist (R,S)-4-phosphonophenylglycine (PPG). Consistent with the lack of signs of epileptic activity in the absence of specific stimuli, mGluR7 -/- mice showed no major changes in synaptic properties in two slice preparations. However, slightly increased excitability was evident in hippocampal slices. In addition, there was slower recovery from frequency facilitation in cortical slices, suggesting a role for mGluR7 as a frequency-dependent regulator in presynaptic terminals. Our findings suggest that mGluR7 receptors have a unique role in regulating neuronal excitability and that these receptors may be a novel target for the development of anticonvulsant drugs."}],"main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6762269/","open_access":"1"}],"doi":"10.1523/JNEUROSCI.21-22-08734.2001","year":"2001","external_id":{"pmid":["11698585"]},"title":"Increased seizure susceptibility in mice lacking metabotropic glutamate receptor 7","page":"8734 - 8745","issue":"22","publication":"Journal of Neuroscience","type":"journal_article","day":"15","status":"public","intvolume":"        21","date_created":"2018-12-11T11:58:39Z","date_published":"2001-11-15T00:00:00Z","article_type":"original","month":"11","language":[{"iso":"eng"}],"publisher":"Society for Neuroscience","scopus_import":"1"},{"date_published":"2001-04-15T00:00:00Z","article_type":"original","month":"04","language":[{"iso":"eng"}],"publisher":"Society for Neuroscience","date_created":"2018-12-11T12:03:37Z","type":"journal_article","day":"15","status":"public","intvolume":"        21","page":"2687 - 2698","issue":"8","publication":"Journal of Neuroscience","doi":"10.1523/JNEUROSCI.21-08-02687.2001","year":"2001","title":"Rapid signaling at inhibitory synapses in a dentate gyrus interneuron network.","external_id":{"pmid":["11306622"]},"main_file_link":[{"url":"ncbi.nlm.nih.gov/pmc/articles/PMC6762544/","open_access":"1"}],"publication_status":"published","citation":{"ista":"Bartos M, Vida I, Frotscher M, Geiger J, Jonas PM. 2001. Rapid signaling at inhibitory synapses in a dentate gyrus interneuron network. Journal of Neuroscience. 21(8), 2687–2698.","short":"M. Bartos, I. Vida, M. Frotscher, J. Geiger, P.M. Jonas, Journal of Neuroscience 21 (2001) 2687–2698.","mla":"Bartos, Marlene, et al. “Rapid Signaling at Inhibitory Synapses in a Dentate Gyrus Interneuron Network.” <i>Journal of Neuroscience</i>, vol. 21, no. 8, Society for Neuroscience, 2001, pp. 2687–98, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.21-08-02687.2001\">10.1523/JNEUROSCI.21-08-02687.2001</a>.","ama":"Bartos M, Vida I, Frotscher M, Geiger J, Jonas PM. Rapid signaling at inhibitory synapses in a dentate gyrus interneuron network. <i>Journal of Neuroscience</i>. 2001;21(8):2687-2698. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.21-08-02687.2001\">10.1523/JNEUROSCI.21-08-02687.2001</a>","chicago":"Bartos, Marlene, Imre Vida, Michael Frotscher, Jörg Geiger, and Peter M Jonas. “Rapid Signaling at Inhibitory Synapses in a Dentate Gyrus Interneuron Network.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2001. <a href=\"https://doi.org/10.1523/JNEUROSCI.21-08-02687.2001\">https://doi.org/10.1523/JNEUROSCI.21-08-02687.2001</a>.","ieee":"M. Bartos, I. Vida, M. Frotscher, J. Geiger, and P. M. Jonas, “Rapid signaling at inhibitory synapses in a dentate gyrus interneuron network.,” <i>Journal of Neuroscience</i>, vol. 21, no. 8. Society for Neuroscience, pp. 2687–2698, 2001.","apa":"Bartos, M., Vida, I., Frotscher, M., Geiger, J., &#38; Jonas, P. M. (2001). Rapid signaling at inhibitory synapses in a dentate gyrus interneuron network. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.21-08-02687.2001\">https://doi.org/10.1523/JNEUROSCI.21-08-02687.2001</a>"},"author":[{"first_name":"Marlene","full_name":"Bartos, Marlene","last_name":"Bartos"},{"last_name":"Vida","full_name":"Vida, Imre","first_name":"Imre"},{"full_name":"Frotscher, Michael","last_name":"Frotscher","first_name":"Michael"},{"full_name":"Geiger, Jörg","last_name":"Geiger","first_name":"Jörg"},{"last_name":"Jonas","full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804","first_name":"Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"}],"abstract":[{"text":"Mutual synaptic interactions between GABAergic interneurons are thought to be of critical importance for the generation of network oscillations and for temporal encoding of information in the hippocampus. However, the functional properties of synaptic transmission between hippocampal interneurons are largely unknown. We have made paired recordings from basket cells (BCs) in the dentate gyrus of rat hippocampal slices, followed by correlated light and electron microscopical analysis. Unitary GABAAreceptor-mediated IPSCs at BC–BC synapses recorded at the soma showed a fast rise and decay, with a mean decay time constant of 2.5 ± 0.2 msec (32°C). Synaptic transmission at BC–BC synapses showed paired-pulse depression (PPD) (32 ± 5% for 10 msec interpulse intervals) and multiple-pulse depression during repetitive stimulation. Detailed passive cable model simulations based on somatodendritic morphology and localization of synaptic contacts further indicated that the conductance change at the postsynaptic site was even faster, decaying with a mean time constant of 1.8 ± 0.6 msec. Sequential triple recordings revealed that the decay time course of IPSCs at BC–BC synapses was approximately twofold faster than that at BC–granule cell synapses, whereas the extent of PPD was comparable. To examine the consequences of the fast postsynaptic conductance change for the generation of oscillatory activity, we developed a computational model of an interneuron network. The model showed robust oscillations at frequencies &gt;60 Hz if the excitatory drive was sufficiently large. Thus the fast conductance change at interneuron–interneuron synapses may promote the generation of high-frequency oscillations observed in the dentate gyrusin vivo. ","lang":"eng"}],"date_updated":"2023-05-15T13:47:04Z","oa":1,"volume":21,"publist_id":"2893","article_processing_charge":"No","acknowledgement":"This work was supported by grants of the Deutsche Forschungsgemeinschaft (SFB 505/C6) and the Human Frontiers Science Program Organization (RG0017/1998-B). We thank Drs. M. V. Jones, J. Bischofberger, and U. Kraushaar for critically reading this manuscript. We also thank B. Taskin and A. Roth for advice in the use of reconstruction and modeling software, and S. Nestel, M. Winter, and A. Blomenkamp for technical assistance.","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","quality_controlled":"1","oa_version":"Published Version","_id":"3494","pmid":1,"publication_identifier":{"issn":["0270-6474"]},"extern":"1"},{"article_processing_charge":"No","publist_id":"2839","oa":1,"date_updated":"2023-05-12T09:47:39Z","volume":21,"extern":"1","publication_identifier":{"issn":["0270-6474"]},"pmid":1,"_id":"3546","quality_controlled":"1","oa_version":"Published Version","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","citation":{"ieee":"H. Hirase, X. Leinekugel, J. L. Csicsvari, A. Czurkó, and G. Buzsáki, “Behavior-dependent states of the hippocampal network affect functional clustering of neurons,” <i>Journal of Neuroscience</i>, vol. 21, no. 10. Society for Neuroscience, 2001.","apa":"Hirase, H., Leinekugel, X., Csicsvari, J. L., Czurkó, A., &#38; Buzsáki, G. (2001). Behavior-dependent states of the hippocampal network affect functional clustering of neurons. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.21-10-j0003.2001\">https://doi.org/10.1523/JNEUROSCI.21-10-j0003.2001</a>","chicago":"Hirase, Hajima, Xavier Leinekugel, Jozsef L Csicsvari, András Czurkó, and György Buzsáki. “Behavior-Dependent States of the Hippocampal Network Affect Functional Clustering of Neurons.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2001. <a href=\"https://doi.org/10.1523/JNEUROSCI.21-10-j0003.2001\">https://doi.org/10.1523/JNEUROSCI.21-10-j0003.2001</a>.","ama":"Hirase H, Leinekugel X, Csicsvari JL, Czurkó A, Buzsáki G. Behavior-dependent states of the hippocampal network affect functional clustering of neurons. <i>Journal of Neuroscience</i>. 2001;21(10). doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.21-10-j0003.2001\">10.1523/JNEUROSCI.21-10-j0003.2001</a>","mla":"Hirase, Hajima, et al. “Behavior-Dependent States of the Hippocampal Network Affect Functional Clustering of Neurons.” <i>Journal of Neuroscience</i>, vol. 21, no. 10, Society for Neuroscience, 2001, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.21-10-j0003.2001\">10.1523/JNEUROSCI.21-10-j0003.2001</a>.","short":"H. Hirase, X. Leinekugel, J.L. Csicsvari, A. Czurkó, G. Buzsáki, Journal of Neuroscience 21 (2001).","ista":"Hirase H, Leinekugel X, Csicsvari JL, Czurkó A, Buzsáki G. 2001. Behavior-dependent states of the hippocampal network affect functional clustering of neurons. Journal of Neuroscience. 21(10)."},"publication_status":"published","abstract":[{"lang":"eng","text":"Local versus distant coherence of hippocampal CA1 pyramidal cells was investigated in the behaving rat. Temporal cross-correlation of pyramidal cells revealed a significantly stronger relationship among local (&lt;140 &lt;mu&gt;m) pyramidal neurons compared with distant (&gt;300 mum) neurons during non-theta-associated immobility and sleep but not during theta-associated running and walking. In contrast, cross-correlation between local pyramidal cell-interneuron pairs was significantly stronger than between distant pairs during theta oscillations but were similar during non-theta-associated behaviors. We suggest that network state-dependent functional clustering of neuronal activity emerges because of the differential contribution of the main excitatory inputs, the perforant path, and Schaffer collaterals during theta and non-theta behaviors."}],"author":[{"last_name":"Hirase","full_name":"Hirase, Hajima","first_name":"Hajima"},{"first_name":"Xavier","full_name":"Leinekugel, Xavier","last_name":"Leinekugel"},{"id":"3FA14672-F248-11E8-B48F-1D18A9856A87","first_name":"Jozsef L","orcid":"0000-0002-5193-4036","full_name":"Csicsvari, Jozsef L","last_name":"Csicsvari"},{"first_name":"András","full_name":"Czurkó, András","last_name":"Czurkó"},{"last_name":"Buzsáki","full_name":"Buzsáki, György","first_name":"György"}],"main_file_link":[{"open_access":"1","url":"https://pubmed.ncbi.nlm.nih.gov/11319243/"}],"year":"2001","doi":"10.1523/JNEUROSCI.21-10-j0003.2001","external_id":{"pmid":["11319243"]},"title":"Behavior-dependent states of the hippocampal network affect functional clustering of neurons","publication":"Journal of Neuroscience","issue":"10","day":"15","type":"journal_article","intvolume":"        21","status":"public","date_created":"2018-12-11T12:03:54Z","month":"05","date_published":"2001-05-15T00:00:00Z","article_type":"original","scopus_import":"1","publisher":"Society for Neuroscience","language":[{"iso":"eng"}]},{"extern":"1","publication_identifier":{"issn":["0270-6474"]},"pmid":1,"_id":"2602","quality_controlled":"1","oa_version":"Published Version","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","acknowledgement":"This work was supported by Centre National de la Recherche Scientifique and grants from Association Française contre les Myopathies, Fondation pour la Recherche Médicale, Bayer (France), and Hoechst-Marrion-Roussel (FRHMR1/9702). We thank J. P. Pin and F. Ango for constructive discussion of this work. We also thank Dr. J. Saugstad (Atlanta, GA) for the rat mGluR7a cDNA, J. M. Sabatier (Marseille, France) for the synthesis of the 68 AA peptide, V. Homburger (Montpellier, France) for the anti-Gαo antibody, and B. Mouillac (Montpellier, France) for the anti-cMyc monoclonal antibody.","article_processing_charge":"No","oa":1,"volume":20,"date_updated":"2023-05-03T09:48:17Z","publist_id":"4296","abstract":[{"lang":"eng","text":"Although presynaptic localization of mGluR7 is well established, the mechanism by which the receptor may control Ca2+ channels in neurons is still unknown. We show here that cultured cerebellar granule cells express native metabotropic glutamate receptor type 7 (mGluR7) in neuritic processes, whereas transfected mGluR7 was also expressed in cell bodies. This allowed us to study the effect of the transfected receptor on somatic Ca2+ channels. In transfected neurons, mGuR7 selectively inhibited P/Q-type Ca2+ channels. The effect was mimicked by GTPγS and blocked by pertussis toxin (PTX) or a selective antibody raised against the G-protein αo subunit, indicating the involvement of a G(o)-like protein. The mGuR7 effect did not display the characteristics of a direct interaction between G-protein βγ subunits and the α1A Ca2+ channel subunit, but was abolished by quenching βγ subunits with specific intracellular peptides. Intracellular dialysis of G-protein βγ subunits did not mimic the action of mGluR7, suggesting that both G-protein βγ and αo subunits were required to mediate the effect. Inhibition of phospholipase C (PLC) blocked the inhibitory action of mGluR7, suggesting that a coincident activation of PLC by the G-protein βγ with αo subunits was required. The Ca2+ chelator BAPTA, as well as inhibition of either the inositol trisphosphate (IP3) receptor or protein kinase C (PKC) abolished the mGluR7 effect. Moreover, activation of native mGluR7 induced a PTX-dependent IP3 formation. These results indicated that IP3-mediated intracellular Ca2+ release was required for PKC-dependent inhibition of the Ca2+ channels. Possible control of synaptic transmission by the present mechanisms is discussed."}],"author":[{"full_name":"Perroy, Julie","last_name":"Perroy","first_name":"Julie"},{"first_name":"Laurent","last_name":"Prezèau","full_name":"Prezèau, Laurent"},{"first_name":"Michel","last_name":"De Waard","full_name":"De Waard, Michel"},{"id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","last_name":"Shigemoto","full_name":"Shigemoto, Ryuichi","orcid":"0000-0001-8761-9444","first_name":"Ryuichi"},{"last_name":"Bockaërt","full_name":"Bockaërt, Joël","first_name":"Joël"},{"last_name":"Fagni","full_name":"Fagni, Laurent","first_name":"Laurent"}],"citation":{"ieee":"J. Perroy, L. Prezèau, M. De Waard, R. Shigemoto, J. Bockaërt, and L. Fagni, “Selective blockade of P/Q-type calcium channels by the metabotropic glutamate receptor type 7 involves a phospholipase C pathway in neurons,” <i>Journal of Neuroscience</i>, vol. 20, no. 21. Society for Neuroscience, pp. 7896–7904, 2000.","apa":"Perroy, J., Prezèau, L., De Waard, M., Shigemoto, R., Bockaërt, J., &#38; Fagni, L. (2000). Selective blockade of P/Q-type calcium channels by the metabotropic glutamate receptor type 7 involves a phospholipase C pathway in neurons. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.20-21-07896.2000\">https://doi.org/10.1523/JNEUROSCI.20-21-07896.2000</a>","chicago":"Perroy, Julie, Laurent Prezèau, Michel De Waard, Ryuichi Shigemoto, Joël Bockaërt, and Laurent Fagni. “Selective Blockade of P/Q-Type Calcium Channels by the Metabotropic Glutamate Receptor Type 7 Involves a Phospholipase C Pathway in Neurons.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2000. <a href=\"https://doi.org/10.1523/JNEUROSCI.20-21-07896.2000\">https://doi.org/10.1523/JNEUROSCI.20-21-07896.2000</a>.","mla":"Perroy, Julie, et al. “Selective Blockade of P/Q-Type Calcium Channels by the Metabotropic Glutamate Receptor Type 7 Involves a Phospholipase C Pathway in Neurons.” <i>Journal of Neuroscience</i>, vol. 20, no. 21, Society for Neuroscience, 2000, pp. 7896–904, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.20-21-07896.2000\">10.1523/JNEUROSCI.20-21-07896.2000</a>.","ama":"Perroy J, Prezèau L, De Waard M, Shigemoto R, Bockaërt J, Fagni L. Selective blockade of P/Q-type calcium channels by the metabotropic glutamate receptor type 7 involves a phospholipase C pathway in neurons. <i>Journal of Neuroscience</i>. 2000;20(21):7896-7904. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.20-21-07896.2000\">10.1523/JNEUROSCI.20-21-07896.2000</a>","short":"J. Perroy, L. Prezèau, M. De Waard, R. Shigemoto, J. Bockaërt, L. Fagni, Journal of Neuroscience 20 (2000) 7896–7904.","ista":"Perroy J, Prezèau L, De Waard M, Shigemoto R, Bockaërt J, Fagni L. 2000. Selective blockade of P/Q-type calcium channels by the metabotropic glutamate receptor type 7 involves a phospholipase C pathway in neurons. Journal of Neuroscience. 20(21), 7896–7904."},"publication_status":"published","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6772734/","open_access":"1"}],"title":"Selective blockade of P/Q-type calcium channels by the metabotropic glutamate receptor type 7 involves a phospholipase C pathway in neurons","external_id":{"pmid":["11050109"]},"year":"2000","doi":"10.1523/JNEUROSCI.20-21-07896.2000","publication":"Journal of Neuroscience","issue":"21","page":"7896 - 7904","intvolume":"        20","status":"public","day":"01","type":"journal_article","date_created":"2018-12-11T11:58:37Z","scopus_import":"1","publisher":"Society for Neuroscience","language":[{"iso":"eng"}],"month":"11","date_published":"2000-11-01T00:00:00Z","article_type":"original"},{"title":"Efficacy and stability of quantal GABA release at a hippocampal interneuron-principal neuron synapse","external_id":{"pmid":["10908596"]},"year":"2000","doi":"10.1523/JNEUROSCI.20-15-05594.2000","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6772523/"}],"abstract":[{"lang":"eng","text":"We have examined factors that determine the strength and dynamics of GABAergic synapses between interneurons [dentate gyrus basket cells (BCs)] and principal neurons [dentate gyrus granule cells (GCs)] using paired recordings in rat hippocampal slices at 34°C. Unitary IPSCs recorded from BC–GC pairs in high intracellular Cl− concentration showed a fast rise and a biexponential decay, with mean time constants of 2 and 9 msec. The mean quantal conductance change, determined directly at reduced extracellular Ca2+/Mg2+concentration ratios, was 1.7 nS. Quantal release at the BC–GC synapse occurred with short delay and was highly synchronized. Analysis of IPSC peak amplitudes and numbers of failures by multiple probability compound binomial analysis indicated that synaptic transmission at the BC–GC synapse involves three to seven release sites, each of which releases transmitter with high probability (∼0.5 in 2 mMCa2+/1 mM Mg2+). Unitary BC–GC IPSCs showed paired-pulse depression (PPD); maximal depression, measured for 10 msec intervals, was 37%, and recovery from depression occurred with a time constant of 2 sec. Paired-pulse depression was mainly presynaptic in origin but appeared to be independent of previous release. Synaptic transmission at the BC–GC synapse showed frequency-dependent depression, with half-maximal decrease at 5 Hz after a series of 1000 presynaptic action potentials. The relative stability of transmission at the BC–GC synapse is consistent with a model in which an activity-dependent gating mechanism reduces release probability and thereby prevents depletion of the releasable pool of synaptic vesicles. Thus several mechanisms converge on the generation of powerful and sustained transmission at interneuron–principal neuron synapses in hippocampal circuits."}],"author":[{"last_name":"Kraushaar","full_name":"Kraushaar, Udo","first_name":"Udo"},{"id":"353C1B58-F248-11E8-B48F-1D18A9856A87","first_name":"Peter M","orcid":"0000-0001-5001-4804","last_name":"Jonas","full_name":"Jonas, Peter M"}],"publication_status":"published","citation":{"chicago":"Kraushaar, Udo, and Peter M Jonas. “Efficacy and Stability of Quantal GABA Release at a Hippocampal Interneuron-Principal Neuron Synapse.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2000. <a href=\"https://doi.org/10.1523/JNEUROSCI.20-15-05594.2000\">https://doi.org/10.1523/JNEUROSCI.20-15-05594.2000</a>.","ieee":"U. Kraushaar and P. M. Jonas, “Efficacy and stability of quantal GABA release at a hippocampal interneuron-principal neuron synapse,” <i>Journal of Neuroscience</i>, vol. 20, no. 15. Society for Neuroscience, pp. 5594–5607, 2000.","apa":"Kraushaar, U., &#38; Jonas, P. M. (2000). Efficacy and stability of quantal GABA release at a hippocampal interneuron-principal neuron synapse. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.20-15-05594.2000\">https://doi.org/10.1523/JNEUROSCI.20-15-05594.2000</a>","ista":"Kraushaar U, Jonas PM. 2000. Efficacy and stability of quantal GABA release at a hippocampal interneuron-principal neuron synapse. Journal of Neuroscience. 20(15), 5594–5607.","short":"U. Kraushaar, P.M. Jonas, Journal of Neuroscience 20 (2000) 5594–5607.","mla":"Kraushaar, Udo, and Peter M. Jonas. “Efficacy and Stability of Quantal GABA Release at a Hippocampal Interneuron-Principal Neuron Synapse.” <i>Journal of Neuroscience</i>, vol. 20, no. 15, Society for Neuroscience, 2000, pp. 5594–607, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.20-15-05594.2000\">10.1523/JNEUROSCI.20-15-05594.2000</a>.","ama":"Kraushaar U, Jonas PM. Efficacy and stability of quantal GABA release at a hippocampal interneuron-principal neuron synapse. <i>Journal of Neuroscience</i>. 2000;20(15):5594-5607. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.20-15-05594.2000\">10.1523/JNEUROSCI.20-15-05594.2000</a>"},"pmid":1,"_id":"3489","extern":"1","publication_identifier":{"issn":["0270-6474"]},"user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","acknowledgement":"This work was supported by grants from the Deutsche Forschungsgemeinschaft (SFB 505/C5) and the Human Frontiers Science Program Organization (RG0017/1998-B) to P.J. Novartis generously provided CGP55845A. We thank Drs. J. Bischofberger, F. A. Edwards, J. R. P. Geiger, M. V. Jones, M. Martina, and A. Roth for critically reading this manuscript. We also thank A. Blomenkamp for technical assistance.","oa_version":"Published Version","quality_controlled":"1","oa":1,"volume":20,"publist_id":"2898","date_updated":"2023-05-03T08:18:39Z","article_processing_charge":"No","publisher":"Society for Neuroscience","scopus_import":"1","language":[{"iso":"eng"}],"month":"08","article_type":"original","date_published":"2000-08-01T00:00:00Z","date_created":"2018-12-11T12:03:36Z","intvolume":"        20","status":"public","day":"01","type":"journal_article","issue":"15","publication":"Journal of Neuroscience","page":"5594 - 5607"},{"date_created":"2018-12-11T12:03:36Z","language":[{"iso":"eng"}],"publisher":"Society for Neuroscience","date_published":"2000-11-15T00:00:00Z","article_type":"original","month":"11","page":"8290 - 8297","issue":"22","publication":"Journal of Neuroscience","status":"public","intvolume":"        20","type":"journal_article","day":"15","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6773198/"}],"external_id":{"pmid":["11069935"]},"title":"Associative long-term depression in the hippocampus is dependent on postsynaptic N-type Ca(2+) channels","doi":"10.1523/JNEUROSCI.20-22-08290.2000","year":"2000","acknowledgement":"This work was supported by a grant from the Deutsche Forschungsgemeinschaft Bi 642/1–2 and University funds (J.B.) and by the Vada and Theodore Stanley Foundation (J.W.). We thank Drs. M. Bartos, J. R. P. Geiger, and M. Martina for critically reading this manuscript and A. Blomenkamp for technical assistance.","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","quality_controlled":"1","oa_version":"Published Version","pmid":1,"_id":"3490","publication_identifier":{"issn":["0270-6474"]},"extern":"1","date_updated":"2023-05-03T08:02:52Z","oa":1,"publist_id":"2897","volume":20,"article_processing_charge":"No","author":[{"last_name":"Normann","full_name":"Normann, Claus","first_name":"Claus"},{"full_name":"Peckys, Diana","last_name":"Peckys","first_name":"Diana"},{"last_name":"Schulze","full_name":"Schulze, Christian","first_name":"Christian"},{"first_name":"Jörg","full_name":"Walden, Jörg","last_name":"Walden"},{"first_name":"Peter M","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Joseph","last_name":"Bischofberger","full_name":"Bischofberger, Joseph"}],"abstract":[{"text":"Long-term depression (LTD) is a form of synaptic plasticity that can be induced either by low-frequency stimulation of presynaptic fibers or in an associative manner by asynchronous pairing of presynaptic and postsynaptic activity. We investigated the induction mechanisms of associative LTD in CA1 pyramidal neurons of the hippocampus using whole-cell patch-clamp recordings and Ca2+ imaging in acute brain slices. Asynchronous pairing of postsynaptic action potentials with EPSPs evoked with a delay of 20 msec induced a robust, long-lasting depression of the EPSP amplitude to 43%. Unlike LTD induced by low-frequency stimulation, associative LTD was resistant to the application of D-AP-5, indicating that it is independent of NMDA receptors. In contrast, associative LTD was inhibited by (S)-α-methyl-4-carboxyphenyl-glycine, indicating the involvement of metabotropic glutamate receptors. Furthermore, associative LTD is dependent on the activation of voltage-gated Ca2+ channels by postsynaptic action potentials. Both nifedipine, an L-type Ca2+ channel antagonist, and ω-conotoxin GVIA, a selective N-type channel blocker, abolished the induction of associative LTD. 8-hydroxy-2-dipropylaminotetralin (OH-DPAT), a 5-HT(1A) receptor agonist, inhibited postsynaptic Ca2+ influx through N-type Ca2+ channels, without affecting presynaptic transmitter release. OH-DPAT also inhibited the induction of associative LTD, suggesting that the involvement of N-type channels makes synaptic plasticity accessible to modulation by neurotransmitters. Thus, the modulation of N-type Ca2+ channels provides a gain control for synaptic depression in hippocampal pyramidal neurons.","lang":"eng"}],"publication_status":"published","citation":{"ama":"Normann C, Peckys D, Schulze C, Walden J, Jonas PM, Bischofberger J. Associative long-term depression in the hippocampus is dependent on postsynaptic N-type Ca(2+) channels. <i>Journal of Neuroscience</i>. 2000;20(22):8290-8297. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.20-22-08290.2000\">10.1523/JNEUROSCI.20-22-08290.2000</a>","mla":"Normann, Claus, et al. “Associative Long-Term Depression in the Hippocampus Is Dependent on Postsynaptic N-Type Ca(2+) Channels.” <i>Journal of Neuroscience</i>, vol. 20, no. 22, Society for Neuroscience, 2000, pp. 8290–97, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.20-22-08290.2000\">10.1523/JNEUROSCI.20-22-08290.2000</a>.","ista":"Normann C, Peckys D, Schulze C, Walden J, Jonas PM, Bischofberger J. 2000. Associative long-term depression in the hippocampus is dependent on postsynaptic N-type Ca(2+) channels. Journal of Neuroscience. 20(22), 8290–8297.","short":"C. Normann, D. Peckys, C. Schulze, J. Walden, P.M. Jonas, J. Bischofberger, Journal of Neuroscience 20 (2000) 8290–8297.","apa":"Normann, C., Peckys, D., Schulze, C., Walden, J., Jonas, P. M., &#38; Bischofberger, J. (2000). Associative long-term depression in the hippocampus is dependent on postsynaptic N-type Ca(2+) channels. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.20-22-08290.2000\">https://doi.org/10.1523/JNEUROSCI.20-22-08290.2000</a>","ieee":"C. Normann, D. Peckys, C. Schulze, J. Walden, P. M. Jonas, and J. Bischofberger, “Associative long-term depression in the hippocampus is dependent on postsynaptic N-type Ca(2+) channels,” <i>Journal of Neuroscience</i>, vol. 20, no. 22. Society for Neuroscience, pp. 8290–8297, 2000.","chicago":"Normann, Claus, Diana Peckys, Christian Schulze, Jörg Walden, Peter M Jonas, and Joseph Bischofberger. “Associative Long-Term Depression in the Hippocampus Is Dependent on Postsynaptic N-Type Ca(2+) Channels.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2000. <a href=\"https://doi.org/10.1523/JNEUROSCI.20-22-08290.2000\">https://doi.org/10.1523/JNEUROSCI.20-22-08290.2000</a>."}},{"date_created":"2018-12-11T11:58:33Z","scopus_import":"1","publisher":"Society for Neuroscience","language":[{"iso":"eng"}],"month":"02","date_published":"1999-02-01T00:00:00Z","article_type":"original","publication":"Journal of Neuroscience","issue":"3","page":"955 - 963","intvolume":"        19","status":"public","day":"01","type":"journal_article","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6782134/"}],"title":"Metabotropic glutamate receptor subtype 7 ablation causes deficit in fear response and conditioned taste aversion","external_id":{"pmid":["9920659"]},"doi":"10.1523/JNEUROSCI.19-03-00955.1999","year":"1999","extern":"1","publication_identifier":{"issn":["0270-6474"]},"pmid":1,"_id":"2592","quality_controlled":"1","oa_version":"Published Version","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","acknowledgement":"This work was supported in part by research grants from the Ministry of Education, Science and Culture of Japan, the Ministry of Health and Welfare of Japan, the Sankyo Foundation, the Yamanouchi Foundation, and the Biomolecular Engineering Research Institute. We thank Takashi Yamamoto for advice on CTA experiments, Fumitaka Ushikubi for advice on the nociception test, Markus Schroeder for back-crossing of mutant mice, Ayae Kinoshita for the kind gift of antibodies, Akira Uesugi for photography, and Kumlesh K. Dev for careful reading of this manuscript.","article_processing_charge":"No","oa":1,"date_updated":"2023-03-27T10:00:42Z","publist_id":"4306","volume":19,"abstract":[{"lang":"eng","text":"Metabotropic glutamate receptors (mGluRs) consist of eight different subtypes and exert their effects or second messengers and ion channels via G- proteins. The function of individual mGluR subtypes in the CNS, however, largely remains to be clarified. We examined the fear response of freezing after electric shock in wild-type and mGluR7(-/-) knockout littermates. Wild- type mice displayed freezing immediately after and 1 d after footshock. In comparison, mGluR7(-/-) knockout mice showed significantly reduced levels in both immediate postshock and delayed freezing responses. However, the knockout mice exhibited no abnormalities in pain sensitivity and locomotor activity. To further examine amygdala-dependent behavior, we performed conditioned taste aversion (CTA) experiments. In wild-type mice, the administration of saccharin followed by intraperitoneal injection of the malaise-inducing agent LiCl resulted in an association between saccharin and LiCl. This association caused strong CTA toward saccharin n contrast, mGluR7(-/-) knockout mice failed to associate between the taste and the negative reinforcer in CTA experiments. Again, the knockout mice showed no abnormalities in taste preference and in the sensitivity to LiCl toxicity. These results indicate that mGluR7 deficiency causes an impairment of two distinct amygdala-dependent behavioral paradigms. Immunohistochemical and immunoelectron-microscopic analyses showed that mGluR7 is highly expressed in amygdala and preferentially localized at the presynaptic axon terminals of glutamatergic neurons. Together, these findings strongly suggest that mGluR7 is involved in neural processes subserving amygdala-dependent averse responses."}],"author":[{"last_name":"Masugi","full_name":"Masugi, Miwako","first_name":"Miwako"},{"full_name":"Yokoi, Mineto","last_name":"Yokoi","first_name":"Mineto"},{"id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8761-9444","last_name":"Shigemoto","full_name":"Shigemoto, Ryuichi","first_name":"Ryuichi"},{"first_name":"Keiko","full_name":"Muguruma, Keiko","last_name":"Muguruma"},{"last_name":"Watanabe","full_name":"Watanabe, Yasuyoshi","first_name":"Yasuyoshi"},{"first_name":"Gilles","full_name":"Sansig, Gilles","last_name":"Sansig"},{"full_name":"Van Der Putten, Herman","last_name":"Van Der Putten","first_name":"Herman"},{"full_name":"Nakanishi, Shigetada","last_name":"Nakanishi","first_name":"Shigetada"}],"citation":{"chicago":"Masugi, Miwako, Mineto Yokoi, Ryuichi Shigemoto, Keiko Muguruma, Yasuyoshi Watanabe, Gilles Sansig, Herman Van Der Putten, and Shigetada Nakanishi. “Metabotropic Glutamate Receptor Subtype 7 Ablation Causes Deficit in Fear Response and Conditioned Taste Aversion.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 1999. <a href=\"https://doi.org/10.1523/JNEUROSCI.19-03-00955.1999\">https://doi.org/10.1523/JNEUROSCI.19-03-00955.1999</a>.","apa":"Masugi, M., Yokoi, M., Shigemoto, R., Muguruma, K., Watanabe, Y., Sansig, G., … Nakanishi, S. (1999). Metabotropic glutamate receptor subtype 7 ablation causes deficit in fear response and conditioned taste aversion. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.19-03-00955.1999\">https://doi.org/10.1523/JNEUROSCI.19-03-00955.1999</a>","ieee":"M. Masugi <i>et al.</i>, “Metabotropic glutamate receptor subtype 7 ablation causes deficit in fear response and conditioned taste aversion,” <i>Journal of Neuroscience</i>, vol. 19, no. 3. Society for Neuroscience, pp. 955–963, 1999.","ista":"Masugi M, Yokoi M, Shigemoto R, Muguruma K, Watanabe Y, Sansig G, Van Der Putten H, Nakanishi S. 1999. Metabotropic glutamate receptor subtype 7 ablation causes deficit in fear response and conditioned taste aversion. Journal of Neuroscience. 19(3), 955–963.","short":"M. Masugi, M. Yokoi, R. Shigemoto, K. Muguruma, Y. Watanabe, G. Sansig, H. Van Der Putten, S. Nakanishi, Journal of Neuroscience 19 (1999) 955–963.","mla":"Masugi, Miwako, et al. “Metabotropic Glutamate Receptor Subtype 7 Ablation Causes Deficit in Fear Response and Conditioned Taste Aversion.” <i>Journal of Neuroscience</i>, vol. 19, no. 3, Society for Neuroscience, 1999, pp. 955–63, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.19-03-00955.1999\">10.1523/JNEUROSCI.19-03-00955.1999</a>.","ama":"Masugi M, Yokoi M, Shigemoto R, et al. Metabotropic glutamate receptor subtype 7 ablation causes deficit in fear response and conditioned taste aversion. <i>Journal of Neuroscience</i>. 1999;19(3):955-963. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.19-03-00955.1999\">10.1523/JNEUROSCI.19-03-00955.1999</a>"},"publication_status":"published"},{"date_created":"2018-12-11T11:58:34Z","scopus_import":"1","publisher":"Society for Neuroscience","language":[{"iso":"eng"}],"month":"05","date_published":"1999-05-01T00:00:00Z","article_type":"original","publication":"Journal of Neuroscience","issue":"9","page":"3545 - 3555","intvolume":"        19","status":"public","day":"01","type":"journal_article","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6782224/","open_access":"1"}],"external_id":{"pmid":["10212314"]},"title":"NK-1 receptor immunoreactivity in distinct morphological types of lamina I neurons of the primate spinal cord","year":"1999","doi":"10.1523/JNEUROSCI.19-09-03545.1999","publication_identifier":{"issn":["0270-6474"]},"extern":"1","pmid":1,"_id":"2593","quality_controlled":"1","oa_version":"None","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","acknowledgement":"This study was supported by National Institute of Health Grants NS 34022 to Y.D.K. and NS 25616 to A.D.C., by Canadian Medical Research Council (MRC) Grants MT 12942 to Y.D.K. and MT 12170 to A.R.S., and by the Barrow Neurological Foundation. Y.D.K. is a Scholar of the Canadian MRC. We thank A. Constantin and A. Forster for expert technical assistance and Dr. M. Wikstrom for generously supplying monoclonal antibodies against CTb.","article_processing_charge":"No","date_updated":"2023-03-27T09:54:40Z","oa":1,"publist_id":"4305","volume":19,"abstract":[{"text":"In cat and monkey, lamina I cells can be classified into three basic morphological types (fusiform, pyramidal, and multipolar), and recent intracellular labeling evidence in the cat indicates that fusiform and multipolar lamina I cells are two different types of nociceptive cells, whereas pyramidal cells are innocuous thermoreceptive-specific. Because earlier observations indicated that only nociceptive dorsal horn neurons respond to substance P (SP), we examined which morphological types of lamina I neurons express receptors for SP (NK-1r). We categorized NK-1r- immunoreactive (IR) lamina I neurons in serial horizontal sections from the cervical and lumbar enlargements of four monkeys. Consistent results were obtained by two independent teams of observers. Nearly all NK-1r-IR cells were fusiform (42%) or multipolar (43%), but only 6% were pyramidal (with 9% unclassified). We obtained similar findings in three monkeys in which we used double-labeling immunocytochemistry to identify NK-1r-IR and spinothalamic lamina I neurons retrogradely labeled with cholera toxin subunit b from the thalamus; most NK-1r-IR lamina I spinothalamic neurons were fusiform (48%) or multipolar (33%), and only 10% were pyramidal. In contrast, most (~75%) pyramidal and some (~25%) fusiform and multipolar lamina I spinothalamic neurons did not display NK-1r immunoreactivity. These data indicate that most fusiform and multipolar lamina I neurons in the monkey can express NK-1r, consistent with the idea that both types are nociceptive, whereas only a small proportion of lamina I pyramidal cells express this receptor, consistent with the previous finding that they are nonnociceptive. However, these findings also indicate that not all nociceptive lamina I neurons express receptors for SP.","lang":"eng"}],"author":[{"first_name":"Xiao","full_name":"Yu, Xiao","last_name":"Yu"},{"first_name":"En","full_name":"Zhang, En","last_name":"Zhang"},{"full_name":"Craig, Arthur","last_name":"Craig","first_name":"Arthur"},{"id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","last_name":"Shigemoto","full_name":"Shigemoto, Ryuichi","orcid":"0000-0001-8761-9444","first_name":"Ryuichi"},{"first_name":"Alfredo","full_name":"Ribeiro Da Silva, Alfredo","last_name":"Ribeiro Da Silva"},{"first_name":"Yves","last_name":"De Koninck","full_name":"De Koninck, Yves"}],"citation":{"apa":"Yu, X., Zhang, E., Craig, A., Shigemoto, R., Ribeiro Da Silva, A., &#38; De Koninck, Y. (1999). NK-1 receptor immunoreactivity in distinct morphological types of lamina I neurons of the primate spinal cord. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.19-09-03545.1999\">https://doi.org/10.1523/JNEUROSCI.19-09-03545.1999</a>","ieee":"X. Yu, E. Zhang, A. Craig, R. Shigemoto, A. Ribeiro Da Silva, and Y. De Koninck, “NK-1 receptor immunoreactivity in distinct morphological types of lamina I neurons of the primate spinal cord,” <i>Journal of Neuroscience</i>, vol. 19, no. 9. Society for Neuroscience, pp. 3545–3555, 1999.","chicago":"Yu, Xiao, En Zhang, Arthur Craig, Ryuichi Shigemoto, Alfredo Ribeiro Da Silva, and Yves De Koninck. “NK-1 Receptor Immunoreactivity in Distinct Morphological Types of Lamina I Neurons of the Primate Spinal Cord.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 1999. <a href=\"https://doi.org/10.1523/JNEUROSCI.19-09-03545.1999\">https://doi.org/10.1523/JNEUROSCI.19-09-03545.1999</a>.","mla":"Yu, Xiao, et al. “NK-1 Receptor Immunoreactivity in Distinct Morphological Types of Lamina I Neurons of the Primate Spinal Cord.” <i>Journal of Neuroscience</i>, vol. 19, no. 9, Society for Neuroscience, 1999, pp. 3545–55, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.19-09-03545.1999\">10.1523/JNEUROSCI.19-09-03545.1999</a>.","ama":"Yu X, Zhang E, Craig A, Shigemoto R, Ribeiro Da Silva A, De Koninck Y. NK-1 receptor immunoreactivity in distinct morphological types of lamina I neurons of the primate spinal cord. <i>Journal of Neuroscience</i>. 1999;19(9):3545-3555. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.19-09-03545.1999\">10.1523/JNEUROSCI.19-09-03545.1999</a>","short":"X. Yu, E. Zhang, A. Craig, R. Shigemoto, A. Ribeiro Da Silva, Y. De Koninck, Journal of Neuroscience 19 (1999) 3545–3555.","ista":"Yu X, Zhang E, Craig A, Shigemoto R, Ribeiro Da Silva A, De Koninck Y. 1999. NK-1 receptor immunoreactivity in distinct morphological types of lamina I neurons of the primate spinal cord. Journal of Neuroscience. 19(9), 3545–3555."},"publication_status":"published"},{"title":"A role for amontillado the Drosophila homolog of the neuropeptide precursor processing protease PC2 in triggering hatching behavior","external_id":{"pmid":["10436051 "]},"doi":"10.1523/jneurosci.19-16-06942.1999","year":"1999","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6782853/"}],"author":[{"first_name":"Daria E","orcid":"0000-0001-8323-8353","full_name":"Siekhaus, Daria E","last_name":"Siekhaus","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Robert","full_name":"Fuller, Robert","last_name":"Fuller"}],"abstract":[{"lang":"eng","text":"Accurate proteolytic processing of neuropeptide and peptide hormone precursors by members of the kexin/furin family of proteases is key to determining both the identities and activities of signaling peptides. Here we identify amontillado (amon), the Drosophila melanogaster homolog of the mammalian neuropeptide processing protease PC2, and show that in contrast to vertebrate PC2, amontillado expression undergoes extensive regulation in the nervous system during development. In situ hybridization reveals that expression of amontillado is restricted to the final stages of embryogenesis when it is found in anterior sensory structures and in only 168 cells in the brain and ventral nerve cord. After larvae hatch from their egg shells, the sensory structures and most cells in the CNS turn off or substantially reduce amontillado expression, suggesting that amontillado plays a specific role late in embryogenesis. Larvae lacking the chromosomal region containing amontillado show no gross anatomical defects and respond to touch. However, such larvae show a greatly reduced frequency of a hatching behavior of wild- type Drosophila in which larvae swing their heads, scraping through the eggshell with their mouth hooks. Ubiquitous expression of amontillado can restore near wild-type levels of this behavior, whereas expression of amontillado with an alanine substitution for the catalytic histidine cannot. These results suggest that amontillado expression is regulated as part of a programmed modulation of neural signaling that controls hatching behavior by producing specific neuropeptides in particular neurons at an appropriate developmental time."}],"publication_status":"published","citation":{"chicago":"Siekhaus, Daria E, and Robert Fuller. “A Role for Amontillado the Drosophila Homolog of the Neuropeptide Precursor Processing Protease PC2 in Triggering Hatching Behavior.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 1999. <a href=\"https://doi.org/10.1523/jneurosci.19-16-06942.1999\">https://doi.org/10.1523/jneurosci.19-16-06942.1999</a>.","apa":"Siekhaus, D. E., &#38; Fuller, R. (1999). A role for amontillado the Drosophila homolog of the neuropeptide precursor processing protease PC2 in triggering hatching behavior. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/jneurosci.19-16-06942.1999\">https://doi.org/10.1523/jneurosci.19-16-06942.1999</a>","ieee":"D. E. Siekhaus and R. Fuller, “A role for amontillado the Drosophila homolog of the neuropeptide precursor processing protease PC2 in triggering hatching behavior,” <i>Journal of Neuroscience</i>, vol. 19, no. 16. Society for Neuroscience, pp. 6942–6954, 1999.","ista":"Siekhaus DE, Fuller R. 1999. A role for amontillado the Drosophila homolog of the neuropeptide precursor processing protease PC2 in triggering hatching behavior. Journal of Neuroscience. 19(16), 6942–6954.","short":"D.E. Siekhaus, R. Fuller, Journal of Neuroscience 19 (1999) 6942–6954.","ama":"Siekhaus DE, Fuller R. A role for amontillado the Drosophila homolog of the neuropeptide precursor processing protease PC2 in triggering hatching behavior. <i>Journal of Neuroscience</i>. 1999;19(16):6942-6954. doi:<a href=\"https://doi.org/10.1523/jneurosci.19-16-06942.1999\">10.1523/jneurosci.19-16-06942.1999</a>","mla":"Siekhaus, Daria E., and Robert Fuller. “A Role for Amontillado the Drosophila Homolog of the Neuropeptide Precursor Processing Protease PC2 in Triggering Hatching Behavior.” <i>Journal of Neuroscience</i>, vol. 19, no. 16, Society for Neuroscience, 1999, pp. 6942–54, doi:<a href=\"https://doi.org/10.1523/jneurosci.19-16-06942.1999\">10.1523/jneurosci.19-16-06942.1999</a>."},"user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","acknowledgement":"This research was supported by National Institutes of Health Grant GM39697 to R.S.F. D.S. was supported in part by National Institutes of Health training Grant 2T32GM07599. We thank M. A. Krasnow and members of his laboratory, particularly J. Jarecki, for technical guidance, encouragement, and stimulating scientific discussions. We thank A. Maghbouleh and the Stanford Statistics Department Consulting Service for help with statistical analysis. We thank G. Beitel, S. Dietrich, K. Guillemin, D. Micklem, Y. Nakajima, and members of the Fuller and Krasnow laboratories for comments on this manuscript. We thank M. Palazzolo for the use of theDrosophila head cDNA library, D. Kiehart for the use of a Drosophila myosin antibody, and D. Casso, F.-A. Ramirez-Weber, and T. B. Kornberg for use of the D/TM3SbKrGFP flies. We thank A. R. Kidd, D. Tolla, and M. Bender and D. Casso, F.-A. Ramirez-Weber and T. B. Kornberg for communication of results before publication","quality_controlled":"1","oa_version":"Published Version","pmid":1,"_id":"3148","extern":"1","publication_identifier":{"issn":["0270-6474"]},"publist_id":"3547","volume":19,"date_updated":"2022-09-07T13:48:41Z","oa":1,"article_processing_charge":"No","language":[{"iso":"eng"}],"publisher":"Society for Neuroscience","scopus_import":"1","date_published":"1999-08-15T00:00:00Z","article_type":"original","month":"08","date_created":"2018-12-11T12:01:40Z","status":"public","intvolume":"        19","type":"journal_article","day":"15","page":"6942 - 6954","issue":"16","publication":"Journal of Neuroscience"},{"date_created":"2018-12-11T12:03:22Z","publisher":"Society for Neuroscience","scopus_import":"1","language":[{"iso":"eng"}],"month":"08","date_published":"1999-08-15T00:00:00Z","article_type":"original","issue":"16","publication":"Journal of Neuroscience","intvolume":"        19","status":"public","day":"15","type":"journal_article","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6782850/","open_access":"1"}],"title":"Fast  network  oscillations  in the  hippocampal  CA1 region of the behaving rat","external_id":{"pmid":["10436076"]},"year":"1999","doi":"10.1523/JNEUROSCI.19-16-j0001.1999","_id":"3444","pmid":1,"extern":"1","publication_identifier":{"issn":["0270-6474"]},"user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","quality_controlled":"1","oa_version":"Published Version","oa":1,"date_updated":"2022-09-07T13:41:18Z","publist_id":"2943","volume":19,"article_processing_charge":"No","abstract":[{"lang":"eng","text":"This study examined intermittent, high-frequency (100-200 Hz) oscillatory patterns in the CA1 region of the hippocampus in the absence of theta activity, i.e., during and in between sharp wave (SPW) bursts. Pyramidal and interneuronal activity was phase-locked not only to large amplitude (&gt;7 SD from baseline) oscillatory events, which are present mainly during SPWs, but to smaller amplitude (&lt;4 SD) patterns, as well. Large-amplitude events were in the 140-200 Hz, &quot;ripple&quot; frequency range. Lower-amplitude events, however, contained slower, 100-130 Hz (&quot;slow&quot;) oscillatory patterns. Fast ripple waves reversed just below the CA1 pyramidal layer, whereas slow oscillatory potentials reversed in the stratum radiatum and/or in the stratum oriens. Parallel CA1-CA3 recordings revealed correlated CA3 field and unit activity to the slow CA1 waves but not to fast ripple waves. These findings suggest that fast ripples emerge in the CA1 region, whereas slow (100-130 Hz) oscillatory patterns are generated in the CA3 region and transferred to the CA1 field."}],"author":[{"id":"3FA14672-F248-11E8-B48F-1D18A9856A87","first_name":"Jozsef L","orcid":"0000-0002-5193-4036","full_name":"Csicsvari, Jozsef L","last_name":"Csicsvari"},{"last_name":"Hirase","full_name":"Hirase, Hajima","first_name":"Hajima"},{"full_name":"Czurkó, András","last_name":"Czurkó","first_name":"András"},{"first_name":"Akira","full_name":"Mamiya, Akira","last_name":"Mamiya"},{"first_name":"György","last_name":"Buzsáki","full_name":"Buzsáki, György"}],"publication_status":"published","citation":{"chicago":"Csicsvari, Jozsef L, Hajima Hirase, András Czurkó, Akira Mamiya, and György Buzsáki. “Fast  Network  Oscillations  in the  Hippocampal  CA1 Region of the Behaving Rat.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 1999. <a href=\"https://doi.org/10.1523/JNEUROSCI.19-16-j0001.1999\">https://doi.org/10.1523/JNEUROSCI.19-16-j0001.1999</a>.","ieee":"J. L. Csicsvari, H. Hirase, A. Czurkó, A. Mamiya, and G. Buzsáki, “Fast  network  oscillations  in the  hippocampal  CA1 region of the behaving rat,” <i>Journal of Neuroscience</i>, vol. 19, no. 16. Society for Neuroscience, 1999.","apa":"Csicsvari, J. L., Hirase, H., Czurkó, A., Mamiya, A., &#38; Buzsáki, G. (1999). Fast  network  oscillations  in the  hippocampal  CA1 region of the behaving rat. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.19-16-j0001.1999\">https://doi.org/10.1523/JNEUROSCI.19-16-j0001.1999</a>","ista":"Csicsvari JL, Hirase H, Czurkó A, Mamiya A, Buzsáki G. 1999. Fast  network  oscillations  in the  hippocampal  CA1 region of the behaving rat. Journal of Neuroscience. 19(16).","short":"J.L. Csicsvari, H. Hirase, A. Czurkó, A. Mamiya, G. Buzsáki, Journal of Neuroscience 19 (1999).","mla":"Csicsvari, Jozsef L., et al. “Fast  Network  Oscillations  in the  Hippocampal  CA1 Region of the Behaving Rat.” <i>Journal of Neuroscience</i>, vol. 19, no. 16, Society for Neuroscience, 1999, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.19-16-j0001.1999\">10.1523/JNEUROSCI.19-16-j0001.1999</a>.","ama":"Csicsvari JL, Hirase H, Czurkó A, Mamiya A, Buzsáki G. Fast  network  oscillations  in the  hippocampal  CA1 region of the behaving rat. <i>Journal of Neuroscience</i>. 1999;19(16). doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.19-16-j0001.1999\">10.1523/JNEUROSCI.19-16-j0001.1999</a>"}}]