[{"fulldoi":"https://doi.org/10.1523/JNEUROSCI.1767-23.2024","status":"public","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_published":"2025-03-26T00:00:00Z","author":[{"full_name":"Stratigi, Aikaterini","last_name":"Stratigi","first_name":"Aikaterini"},{"first_name":"Miguel","full_name":"Soler-García, Miguel","last_name":"Soler-García"},{"first_name":"Mia","full_name":"Krout, Mia","last_name":"Krout"},{"full_name":"Shukla, Shikha","last_name":"Shukla","first_name":"Shikha"},{"id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8347-0443","first_name":"Mario","last_name":"De Bono","full_name":"De Bono, Mario"},{"last_name":"Richmond","full_name":"Richmond, Janet E.","first_name":"Janet E."},{"first_name":"Patrick","last_name":"Laurent","full_name":"Laurent, Patrick"}],"scopus_import":"1","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"acknowledgement":"P.L. is a research associate of the Belgian National Fund for Scientific Research (FRS-FNRS). K.S., M.S.-G., S.S., and P.L. are supported by grants from the FRS-FNRS. This work was supported by an Advanced ERC Grant (269058 ACMO) to M.D.B. We thank the team of Alexander Gottschalk for the snn-1(S9A) strain. We thank the Imaging Facility of the Faculty of Medicine (LiMiF) of the Universite Libre de Bruxelles, supported by FRS-FNRS. This work made use of instruments in the Electron Microscopy Core of the University of Illinois Chicago Research Resources Center as well as the BioCryo facility of Northwestern University's NUANCE Center, which has received support from the SHyNE Resource (NSF ECCS-2025633), the IIN, and Northwestern's MRSEC program (NSF DMR-2308691). Some strains were provided by the CGC, which is funded by NIH Office of Research Infrastructure Programs (P40 OD010440).","oa":1,"file":[{"date_created":"2025-04-07T11:57:19Z","access_level":"open_access","checksum":"7befc0168f4cd5bd2b0fcff9e2a94784","relation":"main_file","file_id":"19525","file_name":"2025_JourNeuroscience_Stratigi.pdf","creator":"dernst","embargo":"2025-09-27","content_type":"application/pdf","date_updated":"2025-09-27T22:30:02Z","file_size":3111735}],"date_created":"2025-04-06T22:01:32Z","quality_controlled":"1","OA_type":"hybrid","OA_place":"publisher","department":[{"_id":"MaDe"}],"oa_version":"Published Version","article_type":"original","OA_embargo":"6 months","article_processing_charge":"No","isi":1,"has_accepted_license":"1","month":"03","doi":"10.1523/JNEUROSCI.1767-23.2024","date_updated":"2026-07-28T11:30:41Z","issue":"13","pmid":1,"citation":{"ieee":"A. Stratigi et al., “Neuroendocrine control of synaptic transmission by PHAC-1 in C. elegans,” Journal of Neuroscience, vol. 45, no. 13. Society for Neuroscience, 2025.","chicago":"Stratigi, Aikaterini, Miguel Soler-García, Mia Krout, Shikha Shukla, Mario de Bono, Janet E. Richmond, and Patrick Laurent. “Neuroendocrine Control of Synaptic Transmission by PHAC-1 in C. Elegans.” Journal of Neuroscience. Society for Neuroscience, 2025. https://doi.org/10.1523/JNEUROSCI.1767-23.2024.","ista":"Stratigi A, Soler-García M, Krout M, Shukla S, de Bono M, Richmond JE, Laurent P. 2025. Neuroendocrine control of synaptic transmission by PHAC-1 in C. elegans. Journal of Neuroscience. 45(13), e1767232024.","short":"A. Stratigi, M. Soler-García, M. Krout, S. Shukla, M. de Bono, J.E. Richmond, P. Laurent, Journal of Neuroscience 45 (2025).","ama":"Stratigi A, Soler-García M, Krout M, et al. Neuroendocrine control of synaptic transmission by PHAC-1 in C. elegans. Journal of Neuroscience. 2025;45(13). doi:10.1523/JNEUROSCI.1767-23.2024","apa":"Stratigi, A., Soler-García, M., Krout, M., Shukla, S., de Bono, M., Richmond, J. E., & Laurent, P. (2025). Neuroendocrine control of synaptic transmission by PHAC-1 in C. elegans. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.1767-23.2024","mla":"Stratigi, Aikaterini, et al. “Neuroendocrine Control of Synaptic Transmission by PHAC-1 in C. Elegans.” Journal of Neuroscience, vol. 45, no. 13, e1767232024, Society for Neuroscience, 2025, doi:10.1523/JNEUROSCI.1767-23.2024."},"intvolume":" 45","abstract":[{"text":"A dynamic interplay between fast synaptic signals and slower neuromodulatory signals controls the excitatory/inhibitory (E/I) balance within neuronal circuits. The mechanisms by which neuropeptide signaling is regulated to maintain E/I balance remain uncertain. We designed a genetic screen to isolate genes involved in the peptidergic maintenance of the E/I balance in the C. elegans motor circuit. This screen identified the C. elegans orthologs of the presynaptic phosphoprotein synapsin (snn-1) and the protein phosphatase 1 (PP1) regulatory subunit PHACTR1 (phac-1). We demonstrate that both phac-1 and snn-1 alter the motor behavior of C. elegans, and genetic interactions suggest that SNN-1 contributes to PP1-PHAC-1 holoenzyme signaling. De novo variants of human PHACTR1, associated with early-onset epilepsies [developmental and epileptic encephalopathy 70 (DEE70)], when expressed in C. elegans resulted in constitutive PP1-PHAC-1 holoenzyme activity. Unregulated PP1-PHAC-1 signaling alters the synapsin and actin cytoskeleton and increases neuropeptide release by cholinergic motor neurons, which secondarily affects the presynaptic vesicle cycle. Together, these results clarify the dominant mechanisms of action of the DEE70 alleles and suggest that altered neuropeptide release may alter E/I balance in DEE70.","lang":"eng"}],"article_number":"e1767232024","publication_identifier":{"issn":["0270-6474"],"eissn":["1529-2401"]},"day":"26","publication_status":"published","ddc":["570"],"type":"journal_article","external_id":{"pmid":["39919830"],"isi":["001460952700001"]},"volume":45,"publisher":"Society for Neuroscience","year":"2025","_id":"19498","file_date_updated":"2025-09-27T22:30:02Z","language":[{"iso":"eng"}],"publication":"Journal of Neuroscience","title":"Neuroendocrine control of synaptic transmission by PHAC-1 in C. elegans"},{"issue":"21","date_updated":"2025-09-08T07:40:58Z","doi":"10.1523/JNEUROSCI.0846-23.2024","citation":{"mla":"Delamare, Geoffroy, et al. “Intrinsic Neural Excitability Biases Allocation and Overlap of Memory Engrams.” Journal of Neuroscience, vol. 44, no. 21, e0846232024, Society for Neuroscience, 2024, doi:10.1523/JNEUROSCI.0846-23.2024.","apa":"Delamare, G., Feitosa Tomé, D., & Clopath, C. (2024). Intrinsic neural excitability biases allocation and overlap of memory engrams. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.0846-23.2024","ama":"Delamare G, Feitosa Tomé D, Clopath C. Intrinsic neural excitability biases allocation and overlap of memory engrams. Journal of Neuroscience. 2024;44(21). doi:10.1523/JNEUROSCI.0846-23.2024","short":"G. Delamare, D. Feitosa Tomé, C. Clopath, Journal of Neuroscience 44 (2024).","ista":"Delamare G, Feitosa Tomé D, Clopath C. 2024. Intrinsic neural excitability biases allocation and overlap of memory engrams. Journal of Neuroscience. 44(21), e0846232024.","ieee":"G. Delamare, D. Feitosa Tomé, and C. Clopath, “Intrinsic neural excitability biases allocation and overlap of memory engrams,” Journal of Neuroscience, vol. 44, no. 21. Society for Neuroscience, 2024.","chicago":"Delamare, Geoffroy, Douglas Feitosa Tomé, and Claudia Clopath. “Intrinsic Neural Excitability Biases Allocation and Overlap of Memory Engrams.” Journal of Neuroscience. Society for Neuroscience, 2024. https://doi.org/10.1523/JNEUROSCI.0846-23.2024."},"pmid":1,"intvolume":" 44","abstract":[{"lang":"eng","text":"Memories are thought to be stored in neural ensembles known as engrams that are specifically reactivated during memory recall. Recent studies have found that memory engrams of two events that happened close in time tend to overlap in the hippocampus and the amygdala, and these overlaps have been shown to support memory linking. It has been hypothesized that engram overlaps arise from the mechanisms that regulate memory allocation itself, involving neural excitability, but the exact process remains unclear. Indeed, most theoretical studies focus on synaptic plasticity and little is known about the role of intrinsic plasticity, which could be mediated by neural excitability and serve as a complementary mechanism for forming memory engrams. Here, we developed a rate-based recurrent neural network that includes both synaptic plasticity and neural excitability. We obtained structural and functional overlap of memory engrams for contexts that are presented close in time, consistent with experimental and computational studies. We then investigated the role of excitability in memory allocation at the network level and unveiled competitive mechanisms driven by inhibition. This work suggests mechanisms underlying the role of intrinsic excitability in memory allocation and linking, and yields predictions regarding the formation and the overlap of memory engrams."}],"article_number":"e0846232024","publication_identifier":{"issn":["0270-6474"],"eissn":["1529-2401"]},"publication_status":"published","day":"22","type":"journal_article","ddc":["570"],"publisher":"Society for Neuroscience","external_id":{"isi":["001249681000008"],"pmid":["38561228"]},"volume":44,"publication":"Journal of Neuroscience","title":"Intrinsic neural excitability biases allocation and overlap of memory engrams","_id":"17092","year":"2024","file_date_updated":"2024-06-03T06:34:21Z","language":[{"iso":"eng"}],"date_published":"2024-05-22T00:00:00Z","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","fulldoi":"https://doi.org/10.1523/JNEUROSCI.0846-23.2024","status":"public","acknowledgement":"We thank Sadra Sadeh and Inês Completo Guerreiro for helpful comments on the manuscript, Yosif Zaki and Denise J. Cai for useful feedback and members of the Clopath lab for discussion and support. This work was supported by Biotechnology and Biological Sciences Research Council (BB/N013956/1 awarded to C.C.), Wellcome Trust (200790/Z/16/Z awarded to C.C.), the Simons Foundation (564408 awarded to C.C.), and Engineering and Physical Sciences Research Council (EP/R035806/1 awarded to C.C.).","author":[{"full_name":"Delamare, Geoffroy","last_name":"Delamare","first_name":"Geoffroy"},{"last_name":"Feitosa Tomé","full_name":"Feitosa Tomé, Douglas","first_name":"Douglas","id":"0eed2d40-3d48-11ec-8d38-f789cc2e40b2"},{"last_name":"Clopath","full_name":"Clopath, Claudia","first_name":"Claudia"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"scopus_import":"1","date_created":"2024-06-02T22:00:57Z","file":[{"success":1,"date_updated":"2024-06-03T06:34:21Z","file_size":920354,"creator":"dernst","content_type":"application/pdf","file_name":"2024_JourNeuroscience_Delamare.pdf","file_id":"17095","access_level":"open_access","date_created":"2024-06-03T06:34:21Z","checksum":"4e19159800db605b802c721e4d4b1ffe","relation":"main_file"}],"oa":1,"article_type":"original","quality_controlled":"1","department":[{"_id":"TiVo"}],"oa_version":"Published Version","isi":1,"article_processing_charge":"Yes (in subscription journal)","has_accepted_license":"1","month":"05"},{"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_published":"2023-06-07T00:00:00Z","status":"public","fulldoi":"https://doi.org/10.1523/JNEUROSCI.1514-22.2023","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.","project":[{"name":"Ultrastructural analysis of phosphoinositides in nerve terminals: distribution, dynamics and physiological roles in synaptic transmission","call_identifier":"H2020","_id":"2659CC84-B435-11E9-9278-68D0E5697425","grant_number":"793482"},{"_id":"25CA28EA-B435-11E9-9278-68D0E5697425","grant_number":"694539","call_identifier":"H2020","name":"In situ analysis of single channel subunit composition in neurons: physiological implication in synaptic plasticity and behaviour"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"scopus_import":"1","author":[{"orcid":"0000-0002-6170-2546","id":"2B7846DC-F248-11E8-B48F-1D18A9856A87","last_name":"Eguchi","full_name":"Eguchi, Kohgaku","first_name":"Kohgaku"},{"id":"3B59276A-F248-11E8-B48F-1D18A9856A87","last_name":"Le Monnier","full_name":"Le Monnier, Elodie","first_name":"Elodie"},{"full_name":"Shigemoto, Ryuichi","last_name":"Shigemoto","first_name":"Ryuichi","orcid":"0000-0001-8761-9444","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87"}],"acknowledged_ssus":[{"_id":"EM-Fac"}],"date_created":"2023-07-09T22:01:12Z","file":[{"date_created":"2023-07-10T09:04:58Z","access_level":"open_access","relation":"main_file","checksum":"70b2141870e0bf1c94fd343e18fdbc32","file_id":"13205","file_name":"2023_JN_Eguchi.pdf","creator":"alisjak","content_type":"application/pdf","date_updated":"2023-07-10T09:04:58Z","success":1,"file_size":7794425}],"oa":1,"article_type":"original","oa_version":"Published Version","department":[{"_id":"RySh"}],"quality_controlled":"1","isi":1,"article_processing_charge":"No","has_accepted_license":"1","month":"06","date_updated":"2025-04-14T07:27:15Z","issue":"23","doi":"10.1523/JNEUROSCI.1514-22.2023","intvolume":" 43","citation":{"mla":"Eguchi, Kohgaku, et al. “Nanoscale Phosphoinositide Distribution on Cell Membranes of Mouse Cerebellar Neurons.” The Journal of Neuroscience, vol. 43, no. 23, Society for Neuroscience, 2023, pp. 4197–216, doi:10.1523/JNEUROSCI.1514-22.2023.","apa":"Eguchi, K., Le Monnier, E., & Shigemoto, R. (2023). Nanoscale phosphoinositide distribution on cell membranes of mouse cerebellar neurons. The Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.1514-22.2023","short":"K. Eguchi, E. Le Monnier, R. Shigemoto, The Journal of Neuroscience 43 (2023) 4197–4216.","ama":"Eguchi K, Le Monnier E, Shigemoto R. Nanoscale phosphoinositide distribution on cell membranes of mouse cerebellar neurons. The Journal of Neuroscience. 2023;43(23):4197-4216. doi:10.1523/JNEUROSCI.1514-22.2023","chicago":"Eguchi, Kohgaku, Elodie Le Monnier, and Ryuichi Shigemoto. “Nanoscale Phosphoinositide Distribution on Cell Membranes of Mouse Cerebellar Neurons.” The Journal of Neuroscience. Society for Neuroscience, 2023. https://doi.org/10.1523/JNEUROSCI.1514-22.2023.","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.","ieee":"K. Eguchi, E. Le Monnier, and R. Shigemoto, “Nanoscale phosphoinositide distribution on cell membranes of mouse cerebellar neurons,” The Journal of Neuroscience, vol. 43, no. 23. Society for Neuroscience, pp. 4197–4216, 2023."},"pmid":1,"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"}],"publication_identifier":{"issn":["0270-6474"],"eissn":["1529-2401"]},"publication_status":"published","day":"07","type":"journal_article","ddc":["570"],"publisher":"Society for Neuroscience","volume":43,"ec_funded":1,"external_id":{"isi":["001020132100005"],"pmid":["37160366"]},"title":"Nanoscale phosphoinositide distribution on cell membranes of mouse cerebellar neurons","corr_author":"1","publication":"The Journal of Neuroscience","language":[{"iso":"eng"}],"page":"4197-4216","file_date_updated":"2023-07-10T09:04:58Z","_id":"13202","year":"2023"},{"date_updated":"2023-08-14T06:56:30Z","issue":"37","doi":"10.1523/JNEUROSCI.0586-21.2021","intvolume":" 41","pmid":1,"citation":{"apa":"Butola, T., Alvanos, T., Hintze, A., Koppensteiner, P., Kleindienst, D., Shigemoto, R., … Moser, T. (2021). RIM-binding protein 2 organizes Ca21 channel topography and regulates release probability and vesicle replenishment at a fast central synapse. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.0586-21.2021","mla":"Butola, Tanvi, et al. “RIM-Binding Protein 2 Organizes Ca21 Channel Topography and Regulates Release Probability and Vesicle Replenishment at a Fast Central Synapse.” Journal of Neuroscience, vol. 41, no. 37, Society for Neuroscience, 2021, pp. 7742–67, doi:10.1523/JNEUROSCI.0586-21.2021.","ieee":"T. Butola et al., “RIM-binding protein 2 organizes Ca21 channel topography and regulates release probability and vesicle replenishment at a fast central synapse,” Journal of Neuroscience, vol. 41, no. 37. Society for Neuroscience, pp. 7742–7767, 2021.","chicago":"Butola, Tanvi, Theocharis Alvanos, Anika Hintze, Peter Koppensteiner, David Kleindienst, Ryuichi Shigemoto, Carolin Wichmann, and Tobias Moser. “RIM-Binding Protein 2 Organizes Ca21 Channel Topography and Regulates Release Probability and Vesicle Replenishment at a Fast Central Synapse.” Journal of Neuroscience. Society for Neuroscience, 2021. https://doi.org/10.1523/JNEUROSCI.0586-21.2021.","ista":"Butola T, Alvanos T, Hintze A, Koppensteiner P, Kleindienst D, Shigemoto R, Wichmann C, Moser T. 2021. RIM-binding protein 2 organizes Ca21 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.","ama":"Butola T, Alvanos T, Hintze A, et al. RIM-binding protein 2 organizes Ca21 channel topography and regulates release probability and vesicle replenishment at a fast central synapse. Journal of Neuroscience. 2021;41(37):7742-7767. doi:10.1523/JNEUROSCI.0586-21.2021"},"abstract":[{"lang":"eng","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."}],"publication_identifier":{"issn":["0270-6474"],"eissn":["1529-2401"]},"publication_status":"published","day":"15","type":"journal_article","ddc":["570"],"publisher":"Society for Neuroscience","volume":41,"external_id":{"pmid":["34353898"],"isi":["000752287700005"]},"title":"RIM-binding protein 2 organizes Ca21 channel topography and regulates release probability and vesicle replenishment at a fast central synapse","publication":"Journal of Neuroscience","language":[{"iso":"eng"}],"page":"7742-7767","file_date_updated":"2022-05-31T09:10:15Z","_id":"10051","year":"2021","date_published":"2021-09-15T00:00:00Z","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","status":"public","fulldoi":"https://doi.org/10.1523/JNEUROSCI.0586-21.2021","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.","scopus_import":"1","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"author":[{"full_name":"Butola, Tanvi","last_name":"Butola","first_name":"Tanvi"},{"first_name":"Theocharis","last_name":"Alvanos","full_name":"Alvanos, Theocharis"},{"first_name":"Anika","full_name":"Hintze, Anika","last_name":"Hintze"},{"id":"3B8B25A8-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-3509-1948","first_name":"Peter","full_name":"Koppensteiner, Peter","last_name":"Koppensteiner"},{"id":"42E121A4-F248-11E8-B48F-1D18A9856A87","full_name":"Kleindienst, David","last_name":"Kleindienst","first_name":"David"},{"id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8761-9444","first_name":"Ryuichi","full_name":"Shigemoto, Ryuichi","last_name":"Shigemoto"},{"first_name":"Carolin","last_name":"Wichmann","full_name":"Wichmann, Carolin"},{"first_name":"Tobias","last_name":"Moser","full_name":"Moser, Tobias"}],"date_created":"2021-09-27T14:33:13Z","file":[{"creator":"dernst","content_type":"application/pdf","success":1,"date_updated":"2022-05-31T09:10:15Z","file_size":11571961,"access_level":"open_access","date_created":"2022-05-31T09:10:15Z","relation":"main_file","checksum":"769ab627c7355a50ccfd445e43a5f351","file_name":"2021_JourNeuroscience_Butola.pdf","file_id":"11423"}],"oa":1,"article_type":"original","oa_version":"Published Version","department":[{"_id":"RySh"}],"quality_controlled":"1","isi":1,"article_processing_charge":"No","has_accepted_license":"1","month":"09"},{"abstract":[{"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.","lang":"eng"}],"publication_identifier":{"eissn":["1529-2401"],"issn":["0270-6474"]},"issue":"5","date_updated":"2025-04-15T08:23:06Z","doi":"10.1523/jneurosci.1655-20.2020","intvolume":" 41","pmid":1,"citation":{"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.","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.” The Journal of Neuroscience. Society for Neuroscience, 2021. https://doi.org/10.1523/jneurosci.1655-20.2020.","ieee":"I. L. Hanganu-Opatz et al., “The logic of developing neocortical circuits in health and disease,” The Journal of Neuroscience, vol. 41, no. 5. Society for Neuroscience, pp. 813–822, 2021.","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.","ama":"Hanganu-Opatz IL, Butt SJB, Hippenmeyer S, et al. The logic of developing neocortical circuits in health and disease. The Journal of Neuroscience. 2021;41(5):813-822. doi:10.1523/jneurosci.1655-20.2020","apa":"Hanganu-Opatz, I. L., Butt, S. J. B., Hippenmeyer, S., De Marco García, N. V., Cardin, J. A., Voytek, B., & Muotri, A. R. (2021). The logic of developing neocortical circuits in health and disease. The Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/jneurosci.1655-20.2020","mla":"Hanganu-Opatz, Ileana L., et al. “The Logic of Developing Neocortical Circuits in Health and Disease.” The Journal of Neuroscience, vol. 41, no. 5, Society for Neuroscience, 2021, pp. 813–22, doi:10.1523/jneurosci.1655-20.2020."},"publisher":"Society for Neuroscience","ec_funded":1,"volume":41,"external_id":{"pmid":["33431633"],"isi":["000616763400002"]},"title":"The logic of developing neocortical circuits in health and disease","publication":"The Journal of Neuroscience","page":"813-822","language":[{"iso":"eng"}],"_id":"9073","file_date_updated":"2022-05-27T06:59:55Z","year":"2021","publication_status":"published","day":"03","type":"journal_article","ddc":["570"],"date_created":"2021-02-03T12:23:51Z","oa":1,"file":[{"file_name":"2021_JourNeuroscience_Hanganu.pdf","file_id":"11414","relation":"main_file","checksum":"578fd7ed1a0aef74bce61bea2d987b33","access_level":"open_access","date_created":"2022-05-27T06:59:55Z","file_size":1031150,"success":1,"date_updated":"2022-05-27T06:59:55Z","content_type":"application/pdf","creator":"dernst"}],"date_published":"2021-02-03T00:00:00Z","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","status":"public","fulldoi":"https://doi.org/10.1523/jneurosci.1655-20.2020","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.","project":[{"grant_number":"725780","_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"},{"_id":"059F6AB4-7A3F-11EA-A408-12923DDC885E","grant_number":"F7805","name":"Stem Cell Modulation in Neural Development and Regeneration/ P05-Molecular Mechanisms of Neural Stem Cell Lineage Progression"}],"scopus_import":"1","author":[{"first_name":"Ileana L.","full_name":"Hanganu-Opatz, Ileana L.","last_name":"Hanganu-Opatz"},{"first_name":"Simon J. B.","last_name":"Butt","full_name":"Butt, Simon J. B."},{"full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","first_name":"Simon","orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Natalia V.","last_name":"De Marco García","full_name":"De Marco García, Natalia V."},{"full_name":"Cardin, Jessica A.","last_name":"Cardin","first_name":"Jessica A."},{"first_name":"Bradley","full_name":"Voytek, Bradley","last_name":"Voytek"},{"first_name":"Alysson R.","full_name":"Muotri, Alysson R.","last_name":"Muotri"}],"has_accepted_license":"1","month":"02","article_type":"original","oa_version":"Published Version","department":[{"_id":"SiHi"}],"quality_controlled":"1","isi":1,"article_processing_charge":"No","keyword":["General Neuroscience"]},{"month":"01","has_accepted_license":"1","article_processing_charge":"No","isi":1,"quality_controlled":"1","department":[{"_id":"GaTk"}],"oa_version":"Published Version","article_type":"original","file":[{"relation":"main_file","date_created":"2020-07-22T11:44:48Z","access_level":"open_access","file_id":"8150","file_name":"2020_JournNeuroscience_Lombardi.pdf","content_type":"application/pdf","creator":"dernst","file_size":6646046,"date_updated":"2020-07-22T11:44:48Z","success":1}],"oa":1,"date_created":"2020-07-05T15:24:51Z","author":[{"first_name":"Fabrizio","last_name":"Lombardi","full_name":"Lombardi, Fabrizio","id":"A057D288-3E88-11E9-986D-0CF4E5697425","orcid":"0000-0003-2623-5249"},{"first_name":"Manuel","full_name":"Gómez-Extremera, Manuel","last_name":"Gómez-Extremera"},{"last_name":"Bernaola-Galván","full_name":"Bernaola-Galván, Pedro","first_name":"Pedro"},{"first_name":"Ramalingam","last_name":"Vetrivelan","full_name":"Vetrivelan, Ramalingam"},{"first_name":"Clifford B.","full_name":"Saper, Clifford B.","last_name":"Saper"},{"last_name":"Scammell","full_name":"Scammell, Thomas E.","first_name":"Thomas E."},{"last_name":"Ivanov","full_name":"Ivanov, Plamen Ch.","first_name":"Plamen Ch."}],"project":[{"name":"ISTplus - Postdoctoral Fellowships","call_identifier":"H2020","_id":"260C2330-B435-11E9-9278-68D0E5697425","grant_number":"754411"}],"scopus_import":"1","status":"public","fulldoi":"https://doi.org/10.1523/jneurosci.1278-19.2019","date_published":"2020-01-02T00:00:00Z","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","_id":"8084","year":"2020","file_date_updated":"2020-07-22T11:44:48Z","language":[{"iso":"eng"}],"page":"171-190","publication":"Journal of Neuroscience","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":{"isi":["000505167600016"],"pmid":["31694962"]},"ec_funded":1,"volume":40,"publisher":"Society for Neuroscience","ddc":["570"],"type":"journal_article","day":"02","publication_status":"published","publication_identifier":{"eissn":["1529-2401"],"issn":["0270-6474"]},"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":{"apa":"Lombardi, F., Gómez-Extremera, M., Bernaola-Galván, P., Vetrivelan, R., Saper, C. B., Scammell, T. E., & 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. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/jneurosci.1278-19.2019","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.” Journal of Neuroscience, vol. 40, no. 1, Society for Neuroscience, 2020, pp. 171–90, doi:10.1523/jneurosci.1278-19.2019.","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.” Journal of Neuroscience. Society for Neuroscience, 2020. https://doi.org/10.1523/jneurosci.1278-19.2019.","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.","ieee":"F. Lombardi 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,” Journal of Neuroscience, vol. 40, no. 1. Society for Neuroscience, pp. 171–190, 2020.","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. Journal of Neuroscience. 2020;40(1):171-190. doi:10.1523/jneurosci.1278-19.2019","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."},"pmid":1,"intvolume":" 40","doi":"10.1523/jneurosci.1278-19.2019","issue":"1","date_updated":"2025-04-14T07:44:04Z"},{"type":"journal_article","ddc":["570"],"publication_status":"published","day":"02","publication":"Journal of neuroscience","title":"Microtubule and actin differentially regulate synaptic vesicle cycling to maintain high-frequency neurotransmission","year":"2020","_id":"7339","file_date_updated":"2020-07-14T12:47:56Z","page":"131-142","language":[{"iso":"eng"}],"publisher":"Society for Neuroscience","external_id":{"isi":["000505167600013"],"pmid":["31767677"]},"volume":40,"pmid":1,"citation":{"ama":"Piriya Ananda Babu L, Wang HY, Eguchi K, Guillaud L, Takahashi T. Microtubule and actin differentially regulate synaptic vesicle cycling to maintain high-frequency neurotransmission. Journal of neuroscience. 2020;40(1):131-142. doi:10.1523/JNEUROSCI.1571-19.2019","short":"L. Piriya Ananda Babu, H.Y. Wang, K. Eguchi, L. Guillaud, T. Takahashi, Journal of Neuroscience 40 (2020) 131–142.","chicago":"Piriya Ananda Babu, Lashmi, Han Ying Wang, Kohgaku Eguchi, Laurent Guillaud, and Tomoyuki Takahashi. “Microtubule and Actin Differentially Regulate Synaptic Vesicle Cycling to Maintain High-Frequency Neurotransmission.” Journal of Neuroscience. Society for Neuroscience, 2020. https://doi.org/10.1523/JNEUROSCI.1571-19.2019.","ista":"Piriya Ananda Babu L, Wang HY, Eguchi K, Guillaud L, Takahashi T. 2020. Microtubule and actin differentially regulate synaptic vesicle cycling to maintain high-frequency neurotransmission. Journal of neuroscience. 40(1), 131–142.","ieee":"L. Piriya Ananda Babu, H. Y. Wang, K. Eguchi, L. Guillaud, and T. Takahashi, “Microtubule and actin differentially regulate synaptic vesicle cycling to maintain high-frequency neurotransmission,” Journal of neuroscience, vol. 40, no. 1. Society for Neuroscience, pp. 131–142, 2020.","mla":"Piriya Ananda Babu, Lashmi, et al. “Microtubule and Actin Differentially Regulate Synaptic Vesicle Cycling to Maintain High-Frequency Neurotransmission.” Journal of Neuroscience, vol. 40, no. 1, Society for Neuroscience, 2020, pp. 131–42, doi:10.1523/JNEUROSCI.1571-19.2019.","apa":"Piriya Ananda Babu, L., Wang, H. Y., Eguchi, K., Guillaud, L., & Takahashi, T. (2020). Microtubule and actin differentially regulate synaptic vesicle cycling to maintain high-frequency neurotransmission. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.1571-19.2019"},"intvolume":" 40","date_updated":"2026-04-16T08:27:29Z","issue":"1","doi":"10.1523/JNEUROSCI.1571-19.2019","publication_identifier":{"eissn":["1529-2401"],"issn":["0270-6474"]},"abstract":[{"lang":"eng","text":"Cytoskeletal filaments such as microtubules (MTs) and filamentous actin (F-actin) dynamically support cell structure and functions. In central presynaptic terminals, F-actin is expressed along the release edge and reportedly plays diverse functional roles, but whether axonal MTs extend deep into terminals and play any physiological role remains controversial. At the calyx of Held in rats of either sex, confocal and high-resolution microscopy revealed that MTs enter deep into presynaptic terminal swellings and partially colocalize with a subset of synaptic vesicles (SVs). Electrophysiological analysis demonstrated that depolymerization of MTs specifically prolonged the slow-recovery time component of EPSCs from short-term depression induced by a train of high-frequency stimulation, whereas depolymerization of F-actin specifically prolonged the fast-recovery component. In simultaneous presynaptic and postsynaptic action potential recordings, depolymerization of MTs or F-actin significantly impaired the fidelity of high-frequency neurotransmission. We conclude that MTs and F-actin differentially contribute to slow and fast SV replenishment, thereby maintaining high-frequency neurotransmission."}],"isi":1,"article_processing_charge":"No","article_type":"original","quality_controlled":"1","department":[{"_id":"RySh"}],"oa_version":"Published Version","month":"01","has_accepted_license":"1","author":[{"first_name":"Lashmi","full_name":"Piriya Ananda Babu, Lashmi","last_name":"Piriya Ananda Babu"},{"first_name":"Han Ying","last_name":"Wang","full_name":"Wang, Han Ying"},{"id":"2B7846DC-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6170-2546","first_name":"Kohgaku","full_name":"Eguchi, Kohgaku","last_name":"Eguchi"},{"first_name":"Laurent","full_name":"Guillaud, Laurent","last_name":"Guillaud"},{"first_name":"Tomoyuki","full_name":"Takahashi, Tomoyuki","last_name":"Takahashi"}],"scopus_import":"1","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"date_published":"2020-01-02T00:00:00Z","user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","status":"public","fulldoi":"https://doi.org/10.1523/JNEUROSCI.1571-19.2019","date_created":"2020-01-19T23:00:38Z","file":[{"file_size":4460781,"date_updated":"2020-07-14T12:47:56Z","content_type":"application/pdf","creator":"dernst","file_name":"2020_JourNeuroscience_Piriya.pdf","file_id":"7345","relation":"main_file","checksum":"92f5e8a47f454fc131fb94cd7f106e60","access_level":"open_access","date_created":"2020-01-20T14:44:10Z"}],"oa":1},{"abstract":[{"lang":"eng","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."}],"publication_identifier":{"issn":["0270-6474","1529-2401"]},"doi":"10.1523/jneurosci.5368-13.2014","issue":"50","date_updated":"2021-01-12T08:06:14Z","pmid":1,"citation":{"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,” Journal of Neuroscience, vol. 34, no. 50. Society for Neuroscience, pp. 16726–16738, 2014.","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.","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.” Journal of Neuroscience. Society for Neuroscience, 2014. https://doi.org/10.1523/jneurosci.5368-13.2014.","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. Journal of Neuroscience. 2014;34(50):16726-16738. doi:10.1523/jneurosci.5368-13.2014","apa":"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. Society for Neuroscience. https://doi.org/10.1523/jneurosci.5368-13.2014","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.” Journal of Neuroscience, vol. 34, no. 50, Society for Neuroscience, 2014, pp. 16726–38, doi:10.1523/jneurosci.5368-13.2014."},"intvolume":" 34","external_id":{"pmid":["25505325"]},"volume":34,"publisher":"Society for Neuroscience","_id":"6126","file_date_updated":"2020-07-14T12:47:20Z","year":"2014","page":"16726-16738","language":[{"iso":"eng"}],"publication":"Journal of Neuroscience","title":"GLOBIN-5-dependent O2 responses are regulated by PDL-1/PrBP that targets prenylated soluble guanylate cyclases to dendritic endings","day":"10","publication_status":"published","ddc":["570"],"type":"journal_article","oa":1,"file":[{"date_created":"2019-03-19T14:55:58Z","access_level":"open_access","relation":"main_file","checksum":"a3dd71969f94c43909327cd083283d4b","file_id":"6127","file_name":"2014_SFN_Gross.pdf","creator":"kschuh","content_type":"application/pdf","date_updated":"2020-07-14T12:47:20Z","file_size":3263422}],"extern":"1","date_created":"2019-03-19T14:52:26Z","status":"public","fulldoi":"https://doi.org/10.1523/jneurosci.5368-13.2014","date_published":"2014-12-10T00:00:00Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"first_name":"E.","full_name":"Gross, E.","last_name":"Gross"},{"first_name":"Z.","last_name":"Soltesz","full_name":"Soltesz, Z."},{"first_name":"S.","full_name":"Oda, S.","last_name":"Oda"},{"full_name":"Zelmanovich, V.","last_name":"Zelmanovich","first_name":"V."},{"first_name":"Z.","full_name":"Abergel, Z.","last_name":"Abergel"},{"first_name":"Mario","full_name":"de Bono, Mario","last_name":"de Bono","id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8347-0443"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"has_accepted_license":"1","month":"12","quality_controlled":"1","oa_version":"Published Version"},{"isi":1,"article_processing_charge":"No","article_type":"original","quality_controlled":"1","department":[{"_id":"RySh"}],"oa_version":"Published Version","month":"11","has_accepted_license":"1","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.","author":[{"first_name":"Hiroshi","full_name":"Matsukawa, Hiroshi","last_name":"Matsukawa"},{"last_name":"Akiyoshi Nishimura","full_name":"Akiyoshi Nishimura, Sachiko","first_name":"Sachiko"},{"first_name":"Qi","full_name":"Zhang, Qi","last_name":"Zhang"},{"first_name":"Rafael","full_name":"Luján, Rafael","last_name":"Luján"},{"first_name":"Kazuhiko","full_name":"Yamaguchi, Kazuhiko","last_name":"Yamaguchi"},{"first_name":"Hiromichi","full_name":"Goto, Hiromichi","last_name":"Goto"},{"full_name":"Yaguchi, Kunio","last_name":"Yaguchi","first_name":"Kunio"},{"first_name":"Tsutomu","last_name":"Hashikawa","full_name":"Hashikawa, Tsutomu"},{"last_name":"Sano","full_name":"Sano, Chie","first_name":"Chie"},{"last_name":"Shigemoto","full_name":"Shigemoto, Ryuichi","first_name":"Ryuichi","orcid":"0000-0001-8761-9444","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Toshiaki","full_name":"Nakashiba, Toshiaki","last_name":"Nakashiba"},{"first_name":"Shigeyoshi","full_name":"Itohara, Shigeyoshi","last_name":"Itohara"}],"scopus_import":"1","date_published":"2014-11-19T00:00:00Z","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","status":"public","fulldoi":"https://doi.org/10.1523/JNEUROSCI.1141-14.2014","date_created":"2018-12-11T11:55:14Z","file":[{"file_id":"11410","file_name":"2014_JournNeuroscience_Matsukawa.pdf","date_created":"2022-05-24T08:41:41Z","access_level":"open_access","relation":"main_file","checksum":"6913e9bc26e9fc1c0441a739a4199229","date_updated":"2022-05-24T08:41:41Z","success":1,"file_size":3963728,"creator":"dernst","content_type":"application/pdf"}],"oa":1,"type":"journal_article","ddc":["570"],"publication_status":"published","day":"19","publication":"Journal of Neuroscience","title":"Netrin-G/NGL complexes encode functional synaptic diversification","year":"2014","_id":"2018","file_date_updated":"2022-05-24T08:41:41Z","language":[{"iso":"eng"}],"page":"15779 - 15792","publisher":"Society for Neuroscience","external_id":{"pmid":["25411505"],"isi":["000345907500026"]},"volume":34,"citation":{"ieee":"H. Matsukawa et al., “Netrin-G/NGL complexes encode functional synaptic diversification,” Journal of Neuroscience, vol. 34, no. 47. Society for Neuroscience, pp. 15779–15792, 2014.","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.","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.” Journal of Neuroscience. Society for Neuroscience, 2014. https://doi.org/10.1523/JNEUROSCI.1141-14.2014.","ama":"Matsukawa H, Akiyoshi Nishimura S, Zhang Q, et al. Netrin-G/NGL complexes encode functional synaptic diversification. Journal of Neuroscience. 2014;34(47):15779-15792. doi:10.1523/JNEUROSCI.1141-14.2014","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.","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. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.1141-14.2014","mla":"Matsukawa, Hiroshi, et al. “Netrin-G/NGL Complexes Encode Functional Synaptic Diversification.” Journal of Neuroscience, vol. 34, no. 47, Society for Neuroscience, 2014, pp. 15779–92, doi:10.1523/JNEUROSCI.1141-14.2014."},"pmid":1,"intvolume":" 34","date_updated":"2025-09-29T12:00:37Z","issue":"47","doi":"10.1523/JNEUROSCI.1141-14.2014","publication_identifier":{"eissn":["1529-2401"],"issn":["0270-6474"]},"publist_id":"5054","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"}]},{"user_id":"D865714E-FA4E-11E9-B85B-F5C5E5697425","date_published":"2011-12-07T00:00:00Z","status":"public","fulldoi":"https://doi.org/10.1523/jneurosci.3894-11.2011","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","orcid":"0000-0003-3295-6181","first_name":"Tim P","full_name":"Vogels, Tim P","last_name":"Vogels"},{"full_name":"Inan, M.","last_name":"Inan","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."}],"extern":"1","date_created":"2020-06-25T13:09:49Z","oa":1,"article_type":"original","quality_controlled":"1","oa_version":"Published Version","article_processing_charge":"No","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4071969/","open_access":"1"}],"month":"12","date_updated":"2021-01-12T08:16:36Z","issue":"49","doi":"10.1523/jneurosci.3894-11.2011","citation":{"short":"A.R. Woodruff, L.M. McGarry, T.P. Vogels, M. Inan, S.A. Anderson, R. Yuste, Journal of Neuroscience 31 (2011) 17872–17886.","ama":"Woodruff AR, McGarry LM, Vogels TP, Inan M, Anderson SA, Yuste R. State-dependent function of neocortical chandelier cells. Journal of Neuroscience. 2011;31(49):17872-17886. doi:10.1523/jneurosci.3894-11.2011","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.” Journal of Neuroscience. Society for Neuroscience, 2011. https://doi.org/10.1523/jneurosci.3894-11.2011.","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.","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,” Journal of Neuroscience, vol. 31, no. 49. Society for Neuroscience, pp. 17872–17886, 2011.","mla":"Woodruff, A. R., et al. “State-Dependent Function of Neocortical Chandelier Cells.” Journal of Neuroscience, vol. 31, no. 49, Society for Neuroscience, 2011, pp. 17872–86, doi:10.1523/jneurosci.3894-11.2011.","apa":"Woodruff, A. R., McGarry, L. M., Vogels, T. P., Inan, M., Anderson, S. A., & Yuste, R. (2011). State-dependent function of neocortical chandelier cells. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/jneurosci.3894-11.2011"},"pmid":1,"intvolume":" 31","abstract":[{"lang":"eng","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."}],"publication_identifier":{"issn":["0270-6474","1529-2401"]},"publication_status":"published","day":"7","type":"journal_article","publisher":"Society for Neuroscience","external_id":{"pmid":["22159102"]},"volume":31,"publication":"Journal of Neuroscience","title":"State-dependent function of neocortical chandelier cells","_id":"8025","year":"2011","page":"17872-17886","language":[{"iso":"eng"}]},{"article_processing_charge":"No","article_type":"original","OA_type":"closed access","oa_version":"None","month":"01","author":[{"full_name":"Doischer, Daniel","last_name":"Doischer","first_name":"Daniel"},{"first_name":"Jonas","last_name":"Hosp","full_name":"Hosp, Jonas"},{"last_name":"Yanagawa","full_name":"Yanagawa, Yuchio","first_name":"Yuchio"},{"full_name":"Obata, Kunihiko","last_name":"Obata","first_name":"Kunihiko"},{"orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","full_name":"Jonas, Peter M","last_name":"Jonas","first_name":"Peter M"},{"full_name":"Vida, Imre","last_name":"Vida","first_name":"Imre"},{"full_name":"Bartos, Marlene","last_name":"Bartos","first_name":"Marlene"}],"date_published":"2008-01-01T00:00:00Z","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","status":"public","fulldoi":"https://doi.org/10.1523/JNEUROSCI.2890-08.2008","extern":"1","date_created":"2018-12-11T12:05:23Z","type":"journal_article","publication_status":"published","day":"01","publication":"The Journal of Neuroscience","title":"Postnatal differentiation of basket cells from slow to fast signaling devices","_id":"3826","year":"2008","page":"12956 - 68","language":[{"iso":"eng"}],"publisher":"Society for Neuroscience","external_id":{"pmid":["19036989"]},"volume":28,"pmid":1,"citation":{"mla":"Doischer, Daniel, et al. “Postnatal Differentiation of Basket Cells from Slow to Fast Signaling Devices.” The Journal of Neuroscience, vol. 28, no. 48, Society for Neuroscience, 2008, pp. 12956–68, doi:10.1523/JNEUROSCI.2890-08.2008.","apa":"Doischer, D., Hosp, J., Yanagawa, Y., Obata, K., Jonas, P. M., Vida, I., & Bartos, M. (2008). Postnatal differentiation of basket cells from slow to fast signaling devices. The Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.2890-08.2008","short":"D. Doischer, J. Hosp, Y. Yanagawa, K. Obata, P.M. Jonas, I. Vida, M. Bartos, The Journal of Neuroscience 28 (2008) 12956–68.","ama":"Doischer D, Hosp J, Yanagawa Y, et al. Postnatal differentiation of basket cells from slow to fast signaling devices. The Journal of Neuroscience. 2008;28(48):12956-12968. doi:10.1523/JNEUROSCI.2890-08.2008","ista":"Doischer D, Hosp J, Yanagawa Y, Obata K, Jonas PM, Vida I, Bartos M. 2008. Postnatal differentiation of basket cells from slow to fast signaling devices. The Journal of Neuroscience. 28(48), 12956–68.","ieee":"D. Doischer et al., “Postnatal differentiation of basket cells from slow to fast signaling devices,” The Journal of Neuroscience, vol. 28, no. 48. Society for Neuroscience, pp. 12956–68, 2008.","chicago":"Doischer, Daniel, Jonas Hosp, Yuchio Yanagawa, Kunihiko Obata, Peter M Jonas, Imre Vida, and Marlene Bartos. “Postnatal Differentiation of Basket Cells from Slow to Fast Signaling Devices.” The Journal of Neuroscience. Society for Neuroscience, 2008. https://doi.org/10.1523/JNEUROSCI.2890-08.2008."},"intvolume":" 28","date_updated":"2026-05-29T10:46:21Z","issue":"48","doi":"10.1523/JNEUROSCI.2890-08.2008","publication_identifier":{"eissn":["1529-2401"],"issn":["0270-6474"]},"publist_id":"2383","abstract":[{"text":"Gamma frequency (30-100 Hz) oscillations in the mature cortex underlie higher cognitive functions. Fast signaling in GABAergic interneuron networks plays a key role in the generation of these oscillations. During development of the rodent brain, gamma activity appears at the end of the first postnatal week, but frequency and synchrony reach adult levels only by the fourth week. However, the mechanisms underlying the maturation of gamma activity are unclear. Here we demonstrate that hippocampal basket cells (BCs), the proposed cellular substrate of gamma oscillations, undergo marked changes in their morphological, intrinsic, and synaptic properties between postnatal day 6 (P6) and P25. During maturation, action potential duration, propagation time, duration of the release period, and decay time constant of IPSCs decreases by approximately 30-60%. Thus, postnatal development converts BCs from slow into fast signaling devices. Computational analysis reveals that BC networks with young intrinsic and synaptic properties as well as reduced connectivity generate oscillations with moderate coherence in the lower gamma frequency range. In contrast, BC networks with mature properties and increased connectivity generate highly coherent activity in the upper gamma frequency band. Thus, late postnatal maturation of BCs enhances coherence in neuronal networks and will thereby contribute to the development of cognitive brain functions.","lang":"eng"}]},{"day":"07","publication_status":"published","type":"journal_article","volume":26,"external_id":{"pmid":["16763040"]},"publisher":"Society for Neuroscience","language":[{"iso":"eng"}],"page":"6318 - 6329","year":"2006","_id":"3545","title":"Changes in functional connectivity within the rat striatopallidal axis during global brain activation in vivo","publication":"Journal of Neuroscience","doi":"10.1523/JNEUROSCI.0620-06.2006","date_updated":"2026-08-28T11:11:24Z","issue":"23","intvolume":" 26","citation":{"apa":"Magill, P., Pogosyan, A., Sharott, A., Csicsvari, J. L., Bolam, J., & Brown, P. (2006). Changes in functional connectivity within the rat striatopallidal axis during global brain activation in vivo. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.0620-06.2006","mla":"Magill, Peter, et al. “Changes in Functional Connectivity within the Rat Striatopallidal Axis during Global Brain Activation in Vivo.” Journal of Neuroscience, vol. 26, no. 23, Society for Neuroscience, 2006, pp. 6318–29, doi:10.1523/JNEUROSCI.0620-06.2006.","chicago":"Magill, Peter, Alek Pogosyan, Andrew Sharott, Jozsef L Csicsvari, John Bolam, and Peter Brown. “Changes in Functional Connectivity within the Rat Striatopallidal Axis during Global Brain Activation in Vivo.” Journal of Neuroscience. Society for Neuroscience, 2006. https://doi.org/10.1523/JNEUROSCI.0620-06.2006.","ieee":"P. Magill, A. Pogosyan, A. Sharott, J. L. Csicsvari, J. Bolam, and P. Brown, “Changes in functional connectivity within the rat striatopallidal axis during global brain activation in vivo,” Journal of Neuroscience, vol. 26, no. 23. Society for Neuroscience, pp. 6318–6329, 2006.","ista":"Magill P, Pogosyan A, Sharott A, Csicsvari JL, Bolam J, Brown P. 2006. Changes in functional connectivity within the rat striatopallidal axis during global brain activation in vivo. Journal of Neuroscience. 26(23), 6318–6329.","ama":"Magill P, Pogosyan A, Sharott A, Csicsvari JL, Bolam J, Brown P. Changes in functional connectivity within the rat striatopallidal axis during global brain activation in vivo. Journal of Neuroscience. 2006;26(23):6318-6329. doi:10.1523/JNEUROSCI.0620-06.2006","short":"P. Magill, A. Pogosyan, A. Sharott, J.L. Csicsvari, J. Bolam, P. Brown, Journal of Neuroscience 26 (2006) 6318–6329."},"pmid":1,"abstract":[{"lang":"eng","text":"The functional organization of the basal ganglia ( BG) is often defined according to one of two opposing schemes. The first proposes multiple, essentially independent channels of information processing. The second posits convergence and lateral integration of striatal channels at the level of the globus pallidus ( GP). We tested the hypothesis that these proposed aspects of functional connectivity within the striatopallidal axis are dynamic and related to brain state. Local field potentials ( LFPs) were simultaneously recorded from multiple sites in striatum and GP in anesthetized rats during slow-wave activity( SWA) and during global activation evoked by sensory stimulation. Functional connectivity was inferred from comparative analyses of the internuclear and intranuclear coherence between bipolar derivations of LFPs. During prominent SWA, as shown in the electrocorticogram and local field potentials in the basal ganglia, intranuclear coherence, and, thus, lateral functional connectivity within striatum or globus pallidus was relatively weak. Furthermore, the temporal coupling of LFPs recorded across these two nuclei involved functional convergence at the level of GP. Global activation, indicated by a loss of SWA, was accompanied by a rapid functional reorganization of the striatopallidal axis. Prominent lateral functional connectivity developed within GP and, to a significantly more constrained spatial extent, striatum. Additionally, functional convergence on GP was no longer apparent, despite increased internuclear coherence. These data demonstrate that functional connectivity within the BG is highly dynamic and suggest that the relative expression of organizational principles, such as parallel, independent processing channels, striatopallidal convergence, and lateral integration within BG nuclei, is dependent on brain state."}],"publist_id":"2840","publication_identifier":{"issn":["0270-6474"],"eissn":["1529-2401"]},"oa_version":"None","OA_type":"closed access","article_type":"original","article_processing_charge":"No","month":"06","status":"public","fulldoi":"https://doi.org/10.1523/JNEUROSCI.0620-06.2006","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","date_published":"2006-06-07T00:00:00Z","author":[{"first_name":"Peter","full_name":"Magill, Peter","last_name":"Magill"},{"last_name":"Pogosyan","full_name":"Pogosyan, Alek","first_name":"Alek"},{"full_name":"Sharott, Andrew","last_name":"Sharott","first_name":"Andrew"},{"orcid":"0000-0002-5193-4036","id":"3FA14672-F248-11E8-B48F-1D18A9856A87","last_name":"Csicsvari","full_name":"Csicsvari, Jozsef L","first_name":"Jozsef L"},{"first_name":"John","full_name":"Bolam, John","last_name":"Bolam"},{"first_name":"Peter","full_name":"Brown, Peter","last_name":"Brown"}],"date_created":"2018-12-11T12:03:53Z","extern":"1"},{"oa":1,"date_created":"2020-06-25T13:12:33Z","extern":"1","author":[{"orcid":"0000-0003-3295-6181","id":"CB6FF8D2-008F-11EA-8E08-2637E6697425","full_name":"Vogels, Tim P","last_name":"Vogels","first_name":"Tim P"},{"last_name":"Abbott","full_name":"Abbott, L. F.","first_name":"L. F."}],"status":"public","fulldoi":"https://doi.org/10.1523/jneurosci.3508-05.2005","user_id":"D865714E-FA4E-11E9-B85B-F5C5E5697425","date_published":"2005-11-16T00:00:00Z","month":"11","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6725859/","open_access":"1"}],"article_processing_charge":"No","oa_version":"Published Version","quality_controlled":"1","article_type":"original","publication_identifier":{"issn":["0270-6474","1529-2401"]},"abstract":[{"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.","lang":"eng"}],"intvolume":" 25","pmid":1,"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.","chicago":"Vogels, Tim P, and L. F. Abbott. “Signal Propagation and Logic Gating in Networks of Integrate-and-Fire Neurons.” Journal of Neuroscience. Society for Neuroscience, 2005. https://doi.org/10.1523/jneurosci.3508-05.2005.","ieee":"T. P. Vogels and L. F. Abbott, “Signal propagation and logic gating in networks of integrate-and-fire neurons,” Journal of Neuroscience, vol. 25, no. 46. Society for Neuroscience, pp. 10786–10795, 2005.","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. Journal of Neuroscience. 2005;25(46):10786-10795. doi:10.1523/jneurosci.3508-05.2005","apa":"Vogels, T. P., & Abbott, L. F. (2005). Signal propagation and logic gating in networks of integrate-and-fire neurons. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/jneurosci.3508-05.2005","mla":"Vogels, Tim P., and L. F. Abbott. “Signal Propagation and Logic Gating in Networks of Integrate-and-Fire Neurons.” Journal of Neuroscience, vol. 25, no. 46, Society for Neuroscience, 2005, pp. 10786–95, doi:10.1523/jneurosci.3508-05.2005."},"doi":"10.1523/jneurosci.3508-05.2005","issue":"46","date_updated":"2021-01-12T08:16:37Z","page":"10786-10795","language":[{"iso":"eng"}],"_id":"8028","year":"2005","title":"Signal propagation and logic gating in networks of integrate-and-fire neurons","publication":"Journal of Neuroscience","volume":25,"external_id":{"pmid":["16291952"]},"publisher":"Society for Neuroscience","type":"journal_article","day":"16","publication_status":"published"},{"date_created":"2018-12-11T11:58:53Z","extern":"1","date_published":"2005-11-09T00:00:00Z","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","status":"public","fulldoi":"https://doi.org/10.1523/JNEUROSCI.2547-05.2005","author":[{"full_name":"Ferraguti, Francesco","last_name":"Ferraguti","first_name":"Francesco"},{"first_name":"Thomas","full_name":"Klausberger, Thomas","last_name":"Klausberger"},{"first_name":"Philip","last_name":"Cobden","full_name":"Cobden, Philip"},{"full_name":"Baude, Agnès","last_name":"Baude","first_name":"Agnès"},{"full_name":"Roberts, John","last_name":"Roberts","first_name":"John"},{"first_name":"Péter","full_name":"Szűcs, Péter","last_name":"Szűcs"},{"first_name":"Ayae","last_name":"Kinoshita","full_name":"Kinoshita, Ayae"},{"orcid":"0000-0001-8761-9444","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","full_name":"Shigemoto, Ryuichi","last_name":"Shigemoto","first_name":"Ryuichi"},{"first_name":"Péter","full_name":"Somogyi, Péter","last_name":"Somogyi"},{"first_name":"Yannis","full_name":"Dalezios, Yannis","last_name":"Dalezios"}],"month":"11","article_type":"original","oa_version":"None","OA_type":"closed access","article_processing_charge":"No","publist_id":"4242","abstract":[{"lang":"eng","text":"Presynaptic metabotropic glutamate receptors (mGluRs) show a highly selective expression and subcellular location in nerve terminals modulating neurotransmitter release. We have demonstrated that alternatively spliced variants of mGluR8, mGluR8a and mGluR8b, have an overlapping distribution in the hippocampus, and besides perforant path terminals, they are expressed in the presynaptic active zone of boutons making synapses selectively with several types of GABAergic interneurons, primarily in the stratum oriens. Boutons labeled for mGluR8 formed either type I or type II synapses, and the latter were GABAergic. Some mGluR8-positive boutons also expressed mGluR7 or vasoactive intestinal polypeptide. Interneurons strongly immunopositive for the muscarinic M2 or the mGlu1 receptors were the primary targets of mGluR8-containing terminals in the stratum oriens, but only neurochemically distinct subsets were innervated by mGluR8-enriched terminals. The majority of M2-positive neurons were mGluR8 innervated, but a minority, which expresses somatostatin, was not. Rare neurons coexpressing calretinin and M2 were consistently targeted by mGluR8-positive boutons. In vivo recording and labeling of an mGluR8-decorated and strongly M2-positive interneuron revealed a trilaminar cell with complex spike bursts during theta oscillations and strong discharge during sharp wave/ripple events. The trilaminar cell had a large projection from the CA1 area to the subiculum and a preferential innervation of interneurons in the CA1 area in addition to pyramidal cell somata and dendrites. The postsynaptic interneuron type-specific expression of the high-efficacy presynaptic mGluR8 in both putative glutamatergic and in identified GABAergic terminals predicts a role in adjusting the activity of interneurons depending on the level of network activity."}],"publication_identifier":{"issn":["0270-6474"],"eissn":["1529-2401"]},"date_updated":"2026-07-29T13:10:21Z","issue":"45","doi":"10.1523/JNEUROSCI.2547-05.2005","intvolume":" 25","citation":{"mla":"Ferraguti, Francesco, et al. “ Metabotropic Glutamate Receptor 8-Expressing Nerve Terminals Target Subsets of GABAergic Neurons in the Hippocampus.” Journal of Neuroscience, vol. 25, no. 45, Society for Neuroscience, 2005, pp. 10520–36, doi:10.1523/JNEUROSCI.2547-05.2005.","apa":"Ferraguti, F., Klausberger, T., Cobden, P., Baude, A., Roberts, J., Szűcs, P., … Dalezios, Y. (2005). Metabotropic glutamate receptor 8-expressing nerve terminals target subsets of GABAergic neurons in the hippocampus. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.2547-05.2005","short":"F. Ferraguti, T. Klausberger, P. Cobden, A. Baude, J. Roberts, P. Szűcs, A. Kinoshita, R. Shigemoto, P. Somogyi, Y. Dalezios, Journal of Neuroscience 25 (2005) 10520–10536.","ama":"Ferraguti F, Klausberger T, Cobden P, et al. Metabotropic glutamate receptor 8-expressing nerve terminals target subsets of GABAergic neurons in the hippocampus. Journal of Neuroscience. 2005;25(45):10520-10536. doi:10.1523/JNEUROSCI.2547-05.2005","chicago":"Ferraguti, Francesco, Thomas Klausberger, Philip Cobden, Agnès Baude, John Roberts, Péter Szűcs, Ayae Kinoshita, Ryuichi Shigemoto, Péter Somogyi, and Yannis Dalezios. “ Metabotropic Glutamate Receptor 8-Expressing Nerve Terminals Target Subsets of GABAergic Neurons in the Hippocampus.” Journal of Neuroscience. Society for Neuroscience, 2005. https://doi.org/10.1523/JNEUROSCI.2547-05.2005.","ista":"Ferraguti F, Klausberger T, Cobden P, Baude A, Roberts J, Szűcs P, Kinoshita A, Shigemoto R, Somogyi P, Dalezios Y. 2005. Metabotropic glutamate receptor 8-expressing nerve terminals target subsets of GABAergic neurons in the hippocampus. Journal of Neuroscience. 25(45), 10520–10536.","ieee":"F. Ferraguti et al., “ Metabotropic glutamate receptor 8-expressing nerve terminals target subsets of GABAergic neurons in the hippocampus,” Journal of Neuroscience, vol. 25, no. 45. Society for Neuroscience, pp. 10520–10536, 2005."},"pmid":1,"publisher":"Society for Neuroscience","volume":25,"external_id":{"pmid":["16280590"]},"title":" Metabotropic glutamate receptor 8-expressing nerve terminals target subsets of GABAergic neurons in the hippocampus","publication":"Journal of Neuroscience","language":[{"iso":"eng"}],"page":"10520 - 10536","_id":"2654","year":"2005","publication_status":"published","day":"09","type":"journal_article"},{"author":[{"first_name":"Christopher","full_name":"Price, Christopher","last_name":"Price"},{"last_name":"Cauli","full_name":"Cauli, Bruno","first_name":"Bruno"},{"full_name":"Kovács, Endre","last_name":"Kovács","first_name":"Endre"},{"full_name":"Kulik, Ákos","last_name":"Kulik","first_name":"Ákos"},{"full_name":"Lambolez, Bertrand","last_name":"Lambolez","first_name":"Bertrand"},{"full_name":"Shigemoto, Ryuichi","last_name":"Shigemoto","first_name":"Ryuichi","orcid":"0000-0001-8761-9444","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Marco","full_name":"Capogna, Marco","last_name":"Capogna"}],"date_published":"2005-07-20T00:00:00Z","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","fulldoi":"https://doi.org/10.1523/JNEUROSCI.1135-05.2005","status":"public","date_created":"2018-12-11T11:58:53Z","extern":"1","article_processing_charge":"No","article_type":"original","oa_version":"None","OA_type":"closed access","month":"07","intvolume":" 25","pmid":1,"citation":{"ieee":"C. Price et al., “Neurogliaform neurons form a novel inhibitory network in the hippocampal CA1 area,” Journal of Neuroscience, vol. 25, no. 29. Society for Neuroscience, pp. 6775–6786, 2005.","ista":"Price C, Cauli B, Kovács E, Kulik Á, Lambolez B, Shigemoto R, Capogna M. 2005. Neurogliaform neurons form a novel inhibitory network in the hippocampal CA1 area. Journal of Neuroscience. 25(29), 6775–6786.","chicago":"Price, Christopher, Bruno Cauli, Endre Kovács, Ákos Kulik, Bertrand Lambolez, Ryuichi Shigemoto, and Marco Capogna. “Neurogliaform Neurons Form a Novel Inhibitory Network in the Hippocampal CA1 Area.” Journal of Neuroscience. Society for Neuroscience, 2005. https://doi.org/10.1523/JNEUROSCI.1135-05.2005.","ama":"Price C, Cauli B, Kovács E, et al. Neurogliaform neurons form a novel inhibitory network in the hippocampal CA1 area. Journal of Neuroscience. 2005;25(29):6775-6786. doi:10.1523/JNEUROSCI.1135-05.2005","short":"C. Price, B. Cauli, E. Kovács, Á. Kulik, B. Lambolez, R. Shigemoto, M. Capogna, Journal of Neuroscience 25 (2005) 6775–6786.","apa":"Price, C., Cauli, B., Kovács, E., Kulik, Á., Lambolez, B., Shigemoto, R., & Capogna, M. (2005). Neurogliaform neurons form a novel inhibitory network in the hippocampal CA1 area. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.1135-05.2005","mla":"Price, Christopher, et al. “Neurogliaform Neurons Form a Novel Inhibitory Network in the Hippocampal CA1 Area.” Journal of Neuroscience, vol. 25, no. 29, Society for Neuroscience, 2005, pp. 6775–86, doi:10.1523/JNEUROSCI.1135-05.2005."},"date_updated":"2026-08-06T13:38:49Z","issue":"29","doi":"10.1523/JNEUROSCI.1135-05.2005","publication_identifier":{"eissn":["1529-2401"],"issn":["0270-6474"]},"publist_id":"4245","abstract":[{"lang":"eng","text":"We studied neurogliaform neurons in the stratum lacunosum moleculare of the CA1 hippocampal area. These interneurons have short stellate dendrites and an extensive axonal arbor mainly located in the stratum lacunosum moleculare. Single-cell reverse transcription-PCR showed that these neurons were GABAergic and that the majority expressed mRNA for neuropeptide Y. Most neurogliaform neurons tested were immunoreactive for α-actinin-2, and many stratum lacunosum moleculare interneurons coexpressed α-actinin-2 and neuropeptide Y. Neurogliaform neurons received monosynaptic, DNQX-sensitive excitatory input from the perforant path, and 40 Hz stimulation of this input evoked EPSCs displaying either depression or initial facilitation, followed by depression. Paired recordings performed between neurogliaform neurons showed that 85% of pairs were electrically connected and 70% were also connected via GABAergic synapses. Injection of sine waveforms into neurons during paired recordings resulted in transmission of the waveforms through the electrical synapse. Unitary IPSCs recorded from neurogliaform pairs readily fatigued, had a slow decay, and had a strong depression of the synaptic response at a 5 Hz stimulation frequency that was antagonized by the GABA B antagonist (2S)-3-[[(1S)-1-(3,4-dichlorophenyl)ethyl]amino-2-hydroxypropyl](phenylmethyl) phosphinic acid (CGP55845). The amplitude of the first IPSC during the 5 Hz stimulation was also increased by CGP55845, suggesting a tonic inhibition of synaptic transmission. A small unitary GABA B-mediated IPSC could also be detected, providing the first evidence for such a component between GABAergic interneurons. Electron microscopic localization of the GABA B1 subunit at neurogliaform synapses revealed the protein in both presynaptic and postsynaptic membranes. Our data disclose a novel interneuronal network well suited for modulating the flow of information between the entorhinal cortex and CA1 hippocampus."}],"type":"journal_article","publication_status":"published","day":"20","title":"Neurogliaform neurons form a novel inhibitory network in the hippocampal CA1 area","publication":"Journal of Neuroscience","page":"6775 - 6786","language":[{"iso":"eng"}],"_id":"2652","year":"2005","publisher":"Society for Neuroscience","volume":25,"external_id":{"pmid":["16033887"]}},{"pmid":1,"citation":{"apa":"Wu, Y., Kawakami, R., Shinohara, Y., Fukaya, M., Sakimura, K., Mishina, M., … Shigemoto, R. (2005). Target-cell-specific left-right asymmetry of NMDA receptor content in Schaffer collateral synapses in ε1/NR2A knock-out mice. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.2134-05.2005","mla":"Wu, Yue, et al. “Target-Cell-Specific Left-Right Asymmetry of NMDA Receptor Content in Schaffer Collateral Synapses in Ε1/NR2A Knock-out Mice.” Journal of Neuroscience, vol. 25, no. 40, Society for Neuroscience, 2005, pp. 9213–26, doi:10.1523/JNEUROSCI.2134-05.2005.","ista":"Wu Y, Kawakami R, Shinohara Y, Fukaya M, Sakimura K, Mishina M, Watanabe M, Ito I, Shigemoto R. 2005. Target-cell-specific left-right asymmetry of NMDA receptor content in Schaffer collateral synapses in ε1/NR2A knock-out mice. Journal of Neuroscience. 25(40), 9213–9226.","ieee":"Y. Wu et al., “Target-cell-specific left-right asymmetry of NMDA receptor content in Schaffer collateral synapses in ε1/NR2A knock-out mice,” Journal of Neuroscience, vol. 25, no. 40. Society for Neuroscience, pp. 9213–9226, 2005.","chicago":"Wu, Yue, Ryosuke Kawakami, Yoshiaki Shinohara, Masahiro Fukaya, Kenji Sakimura, Masayoshi Mishina, Masahiko Watanabe, Isao Ito, and Ryuichi Shigemoto. “Target-Cell-Specific Left-Right Asymmetry of NMDA Receptor Content in Schaffer Collateral Synapses in Ε1/NR2A Knock-out Mice.” Journal of Neuroscience. Society for Neuroscience, 2005. https://doi.org/10.1523/JNEUROSCI.2134-05.2005.","short":"Y. Wu, R. Kawakami, Y. Shinohara, M. Fukaya, K. Sakimura, M. Mishina, M. Watanabe, I. Ito, R. Shigemoto, Journal of Neuroscience 25 (2005) 9213–9226.","ama":"Wu Y, Kawakami R, Shinohara Y, et al. Target-cell-specific left-right asymmetry of NMDA receptor content in Schaffer collateral synapses in ε1/NR2A knock-out mice. Journal of Neuroscience. 2005;25(40):9213-9226. doi:10.1523/JNEUROSCI.2134-05.2005"},"intvolume":" 25","issue":"40","date_updated":"2026-08-06T13:30:33Z","doi":"10.1523/JNEUROSCI.2134-05.2005","publication_identifier":{"eissn":["1529-2401"],"issn":["0270-6474"]},"publist_id":"4243","abstract":[{"text":"Input-dependent left-right asymmetry of NMDA receptor ε2 (NR2B) subunit allocation was discovered in hippocampal Schaffer collateral (Sch) and commissural fiber pyramidal cell synapses (Kawakami et al., 2003). To investigate whether this asymmetrical ε2 allocation is also related to the types of the postsynaptic cells, we compared postembedding immunogold labeling for ε2 in left and right Sch synapses on pyramidal cells and interneurons. To facilitate the detection of ε2 density difference, we used ε1 (NR2A) knock-out (KO) mice, which have a simplified NMDA receptor subunit composition. The labeling density for ε2 but not ζ1 (NR1) and subtype 2/3 glutamate receptor (GluR2/3) in Sch-CA1 pyramidal cell synapses was significantly different between the left and right hippocampus with opposite directions in strata oriens and radiatum; the left to right ratio of ε2 labeling density was 1:1.50 in stratum oriens and 1.44:1 in stratum radiatum. No significant difference, however, was detected in CA1 stratum radiatum between the left and right Sch-GluR4-positive (mostly parvalbumin-positive) and Sch-GluR4-negative interneuron synapses. Consistent with the anatomical asymmetry, the amplitude ratio of NMDA EPSCs to non-NMDA EPSCs in pyramidal cells was approximately two times larger in right than left stratum radiatum and vice versa in stratum oriens of ε1 KO mice. Moreover, the amplitude of long-term potentiation in the Sch-CA1 synapses of left stratum radiatum was significantly larger than that in the right corresponding synapses. These results indicate that the asymmetry of ε2 distribution is target cell specific, resulting in the left-right difference in NMDA receptor content and plasticity in Sch-CA1 pyramidal cell synapses in ε1 KO mice.","lang":"eng"}],"type":"journal_article","publication_status":"published","day":"05","publication":"Journal of Neuroscience","title":"Target-cell-specific left-right asymmetry of NMDA receptor content in Schaffer collateral synapses in ε1/NR2A knock-out mice","year":"2005","_id":"2655","page":"9213 - 9226","language":[{"iso":"eng"}],"publisher":"Society for Neuroscience","external_id":{"pmid":["16207881 "]},"volume":25,"author":[{"full_name":"Wu, Yue","last_name":"Wu","first_name":"Yue"},{"full_name":"Kawakami, Ryosuke","last_name":"Kawakami","first_name":"Ryosuke"},{"first_name":"Yoshiaki","full_name":"Shinohara, Yoshiaki","last_name":"Shinohara"},{"first_name":"Masahiro","full_name":"Fukaya, Masahiro","last_name":"Fukaya"},{"full_name":"Sakimura, Kenji","last_name":"Sakimura","first_name":"Kenji"},{"last_name":"Mishina","full_name":"Mishina, Masayoshi","first_name":"Masayoshi"},{"full_name":"Watanabe, Masahiko","last_name":"Watanabe","first_name":"Masahiko"},{"full_name":"Ito, Isao","last_name":"Ito","first_name":"Isao"},{"id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8761-9444","first_name":"Ryuichi","last_name":"Shigemoto","full_name":"Shigemoto, Ryuichi"}],"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","date_published":"2005-10-05T00:00:00Z","fulldoi":"https://doi.org/10.1523/JNEUROSCI.2134-05.2005","status":"public","extern":"1","date_created":"2018-12-11T11:58:54Z","article_processing_charge":"No","article_type":"original","OA_type":"closed access","oa_version":"None","month":"10"},{"issue":"19","date_updated":"2026-08-14T10:30:59Z","doi":"10.1523/JNEUROSCI.4900-04.2005","intvolume":" 25","citation":{"ista":"Reiff D, Ihring A, Guerrero G, Isacoff E, Jösch MA, Nakai J, Borst A. 2005. In vivo performance of genetically encoded indicators of neural activity in flies. Journal of Neuroscience. 25(19), 4766–4778.","chicago":"Reiff, Dierk, Alexandra Ihring, Giovanna Guerrero, Ehud Isacoff, Maximilian A Jösch, Junichi Nakai, and Alexander Borst. “In Vivo Performance of Genetically Encoded Indicators of Neural Activity in Flies.” Journal of Neuroscience. Society for Neuroscience, 2005. https://doi.org/10.1523/JNEUROSCI.4900-04.2005.","ieee":"D. Reiff et al., “In vivo performance of genetically encoded indicators of neural activity in flies,” Journal of Neuroscience, vol. 25, no. 19. Society for Neuroscience, pp. 4766–4778, 2005.","ama":"Reiff D, Ihring A, Guerrero G, et al. In vivo performance of genetically encoded indicators of neural activity in flies. Journal of Neuroscience. 2005;25(19):4766-4778. doi:10.1523/JNEUROSCI.4900-04.2005","short":"D. Reiff, A. Ihring, G. Guerrero, E. Isacoff, M.A. Jösch, J. Nakai, A. Borst, Journal of Neuroscience 25 (2005) 4766–4778.","apa":"Reiff, D., Ihring, A., Guerrero, G., Isacoff, E., Jösch, M. A., Nakai, J., & Borst, A. (2005). In vivo performance of genetically encoded indicators of neural activity in flies. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.4900-04.2005","mla":"Reiff, Dierk, et al. “In Vivo Performance of Genetically Encoded Indicators of Neural Activity in Flies.” Journal of Neuroscience, vol. 25, no. 19, Society for Neuroscience, 2005, pp. 4766–78, doi:10.1523/JNEUROSCI.4900-04.2005."},"pmid":1,"publist_id":"5975","abstract":[{"text":"Genetically encoded fluorescent probes of neural activity represent new promising tools for systems neuroscience. Here, we present a comparative in vivo analysis of 10 different genetically encoded calcium indicators, as well as the pH-sensitive synapto-pHluorin. We analyzed their fluorescence changes in presynaptic boutons of the Drosophila larval neuromuscular junction. Robust neural activity did not result in any or noteworthy fluorescence changes when Flash-Pericam, Camgaroo-1, and Camgaroo-2 were expressed. However, calculated on the raw data, fractional fluorescence changes up to 18% were reported by synapto-pHluorin, Yellow Cameleon 2.0, 2.3, and 3.3, Inverse-Pericam, GCaMP1.3, GCaMP1.6, and the troponin C-based calcium sensor TN-L15. The response characteristics of all of these indicators differed considerably from each other, with GCaMP1.6 reporting high rates of neural activity with the largest and fastest fluorescence changes. However, GCaMP1.6 suffered from photobleaching, whereas the fluorescence signals of the double-chromophore indicators were in general smaller but more photostable and reproducible, with TN-L15 showing the fastest rise of the signals at lower activity rates. We show for GCaMP1.3 and YC3.3 that an expanded range of neural activity evoked fairly linear fluorescence changes and a corresponding linear increase in the signal-to-noise ratio (SNR). The expression level of the indicator biased the signal kinetics and SNR, whereas the signal amplitude was independent. The presented data will be useful for in vivo experiments with respect to the selection of an appropriate indicator, as well as for the correct interpretation of the optical signals.","lang":"eng"}],"publication_identifier":{"eissn":["1529-2401"],"issn":["0270-6474"]},"publication_status":"published","day":"11","type":"journal_article","publisher":"Society for Neuroscience","volume":25,"external_id":{"pmid":["15888652"]},"title":"In vivo performance of genetically encoded indicators of neural activity in flies","publication":"Journal of Neuroscience","language":[{"iso":"eng"}],"page":"4766 - 4778","_id":"1298","year":"2005","date_published":"2005-03-11T00:00:00Z","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","status":"public","fulldoi":"https://doi.org/10.1523/JNEUROSCI.4900-04.2005","acknowledgement":"This work was supported by the Max-Planck-Society.","author":[{"first_name":"Dierk","last_name":"Reiff","full_name":"Reiff, Dierk"},{"first_name":"Alexandra","last_name":"Ihring","full_name":"Ihring, Alexandra"},{"first_name":"Giovanna","full_name":"Guerrero, Giovanna","last_name":"Guerrero"},{"last_name":"Isacoff","full_name":"Isacoff, Ehud","first_name":"Ehud"},{"full_name":"Jösch, Maximilian A","last_name":"Jösch","first_name":"Maximilian A","orcid":"0000-0002-3937-1330","id":"2BD278E6-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Junichi","full_name":"Nakai, Junichi","last_name":"Nakai"},{"last_name":"Borst","full_name":"Borst, Alexander","first_name":"Alexander"}],"date_created":"2018-12-11T11:51:13Z","extern":"1","article_type":"original","oa_version":"None","OA_type":"closed access","article_processing_charge":"No","month":"03"},{"doi":"10.1523/JNEUROSCI.2162-04.2004","issue":"44","date_updated":"2026-09-22T13:15:36Z","intvolume":" 24","citation":{"mla":"Chan, Savio, et al. “HCN2 and HCN1 Channels Govern the Regularity of Autonomous Pacemaking and Synaptic Resetting in Globus Pallidus Neurons.” Journal of Neuroscience, vol. 24, no. 44, Society for Neuroscience, 2004, pp. 9921–32, doi:10.1523/JNEUROSCI.2162-04.2004.","apa":"Chan, S., Shigemoto, R., Mercer, J., & Surmeier, J. (2004). HCN2 and HCN1 channels govern the regularity of autonomous pacemaking and synaptic resetting in globus pallidus neurons. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.2162-04.2004","ama":"Chan S, Shigemoto R, Mercer J, Surmeier J. HCN2 and HCN1 channels govern the regularity of autonomous pacemaking and synaptic resetting in globus pallidus neurons. Journal of Neuroscience. 2004;24(44):9921-9932. doi:10.1523/JNEUROSCI.2162-04.2004","short":"S. Chan, R. Shigemoto, J. Mercer, J. Surmeier, Journal of Neuroscience 24 (2004) 9921–9932.","ieee":"S. Chan, R. Shigemoto, J. Mercer, and J. Surmeier, “HCN2 and HCN1 channels govern the regularity of autonomous pacemaking and synaptic resetting in globus pallidus neurons,” Journal of Neuroscience, vol. 24, no. 44. Society for Neuroscience, pp. 9921–9932, 2004.","ista":"Chan S, Shigemoto R, Mercer J, Surmeier J. 2004. HCN2 and HCN1 channels govern the regularity of autonomous pacemaking and synaptic resetting in globus pallidus neurons. Journal of Neuroscience. 24(44), 9921–9932.","chicago":"Chan, Savio, Ryuichi Shigemoto, Jeff Mercer, and James Surmeier. “HCN2 and HCN1 Channels Govern the Regularity of Autonomous Pacemaking and Synaptic Resetting in Globus Pallidus Neurons.” Journal of Neuroscience. Society for Neuroscience, 2004. https://doi.org/10.1523/JNEUROSCI.2162-04.2004."},"pmid":1,"abstract":[{"lang":"eng","text":"The globus pallidus (GP) is a critical component of the basal ganglia circuitry controlling motor behavior. Dysregulation of GP activity has been implicated in a number of psychomotor disorders, including Parkinson's disease (PD), in which a cardinal feature of the pathophysiology is an alteration in the pattern and synchrony of discharge in GP neurons. Yet the determinants of this activity in GP neurons are poorly understood. To help fill this gap, electrophysiological, molecular, and computational approaches were used to identify and characterize GABAergic GP neurons in tissue slices from rodents. In vitro, GABAergic GP neurons generate a regular, autonomous, single-spike pacemaker activity. Hyperpolarization-activated, cyclic nucleotide-gated cation (HCN) channels make an important contribution to this process: their blockade with ZD7288 significantly slowed discharge rate and decreased its regularity. HCN currents evoked by somatic voltage clamp had fast and slow components. Single-cell RT-PCR and immunohistochemical approaches revealed robust expression of HCN2 subunits as well as significant levels of HCN1 subunits in GABAergic GP neurons. Transient activation of striatal GABAergic input to GP neurons led to a resetting of rhythmic discharge that was dependent on HCN currents. Simulations suggested that the ability of transient striatal GABAergic input to reset pacemaking was dependent on dendritic HCN2/HCN1 channels. Together, these studies show that HCN channels in GABAergic GP neurons are key determinants of the regularity and rate of pacemaking as well as striatal resetting of this activity, implicating HCN channels in the emergence of synchrony in PD."}],"publist_id":"4252","publication_identifier":{"issn":["0270-6474"],"eissn":["1529-2401"]},"day":"03","publication_status":"published","type":"journal_article","volume":24,"external_id":{"pmid":["15525777"]},"publisher":"Society for Neuroscience","language":[{"iso":"eng"}],"page":"9921 - 9932","_id":"2645","year":"2004","title":"HCN2 and HCN1 channels govern the regularity of autonomous pacemaking and synaptic resetting in globus pallidus neurons","publication":"Journal of Neuroscience","status":"public","fulldoi":"https://doi.org/10.1523/JNEUROSCI.2162-04.2004","date_published":"2004-11-03T00:00:00Z","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","author":[{"full_name":"Chan, Savio","last_name":"Chan","first_name":"Savio"},{"id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8761-9444","first_name":"Ryuichi","full_name":"Shigemoto, Ryuichi","last_name":"Shigemoto"},{"first_name":"Jeff","full_name":"Mercer, Jeff","last_name":"Mercer"},{"first_name":"James","last_name":"Surmeier","full_name":"Surmeier, James"}],"date_created":"2018-12-11T11:58:51Z","extern":"1","oa_version":"None","OA_type":"closed access","article_type":"original","article_processing_charge":"No","month":"11"},{"OA_type":"closed access","oa_version":"None","article_type":"original","article_processing_charge":"No","month":"04","fulldoi":"https://doi.org/10.1523/JNEUROSCI.5641-03.2004","status":"public","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","date_published":"2004-04-07T00:00:00Z","author":[{"first_name":"Youngnam","full_name":"Kang, Youngnam","last_name":"Kang"},{"first_name":"Takuya","last_name":"Notomi","full_name":"Notomi, Takuya"},{"last_name":"Saito","full_name":"Saito, Mitsuru","first_name":"Mitsuru"},{"first_name":"Wei","full_name":"Zhang, Wei","last_name":"Zhang"},{"id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8761-9444","first_name":"Ryuichi","full_name":"Shigemoto, Ryuichi","last_name":"Shigemoto"}],"extern":"1","date_created":"2018-12-11T11:58:49Z","day":"07","publication_status":"published","type":"journal_article","external_id":{"pmid":["15071118"]},"volume":24,"publisher":"Society for Neuroscience","year":"2004","_id":"2641","page":"3694 - 3702","language":[{"iso":"eng"}],"publication":"Journal of Neuroscience","title":"Bidirectional interactions between H-channels and Na+-K + pumps in mesencephalic trigeminal neurons","doi":"10.1523/JNEUROSCI.5641-03.2004","issue":"14","date_updated":"2026-09-22T13:22:20Z","pmid":1,"citation":{"mla":"Kang, Youngnam, et al. “Bidirectional Interactions between H-Channels and Na+-K + Pumps in Mesencephalic Trigeminal Neurons.” Journal of Neuroscience, vol. 24, no. 14, Society for Neuroscience, 2004, pp. 3694–702, doi:10.1523/JNEUROSCI.5641-03.2004.","apa":"Kang, Y., Notomi, T., Saito, M., Zhang, W., & Shigemoto, R. (2004). Bidirectional interactions between H-channels and Na+-K + pumps in mesencephalic trigeminal neurons. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.5641-03.2004","ama":"Kang Y, Notomi T, Saito M, Zhang W, Shigemoto R. Bidirectional interactions between H-channels and Na+-K + pumps in mesencephalic trigeminal neurons. Journal of Neuroscience. 2004;24(14):3694-3702. doi:10.1523/JNEUROSCI.5641-03.2004","short":"Y. Kang, T. Notomi, M. Saito, W. Zhang, R. Shigemoto, Journal of Neuroscience 24 (2004) 3694–3702.","ieee":"Y. Kang, T. Notomi, M. Saito, W. Zhang, and R. Shigemoto, “Bidirectional interactions between H-channels and Na+-K + pumps in mesencephalic trigeminal neurons,” Journal of Neuroscience, vol. 24, no. 14. Society for Neuroscience, pp. 3694–3702, 2004.","chicago":"Kang, Youngnam, Takuya Notomi, Mitsuru Saito, Wei Zhang, and Ryuichi Shigemoto. “Bidirectional Interactions between H-Channels and Na+-K + Pumps in Mesencephalic Trigeminal Neurons.” Journal of Neuroscience. Society for Neuroscience, 2004. https://doi.org/10.1523/JNEUROSCI.5641-03.2004.","ista":"Kang Y, Notomi T, Saito M, Zhang W, Shigemoto R. 2004. Bidirectional interactions between H-channels and Na+-K + pumps in mesencephalic trigeminal neurons. Journal of Neuroscience. 24(14), 3694–3702."},"intvolume":" 24","abstract":[{"text":"The Na+-K+ pump current (Ip) and the h-current (Ih) flowing through hyperpolarization-activated channels (h-channels) participate in generating the resting potential. These two currents are thought to be produced independently. We show here bidirectional interactions between Na+-K+ pumps and h-channels in mesencephalic trigeminal neurons. Activation of Ih leads to the generation of two types of ouabain-sensitive Ip with temporal profiles similar to those of instantaneous and slow components of I h, presumably reflecting Na+ transients in a restricted cellular space. Moreover, the Ip activated by instantaneous I h can facilitate the subsequent activation of slow Ih. Such counteractive and cooperative interactions were also disclosed by replacing extracellular Na+ with Li+, which is permeant through h-channels but does not stimulate the Na+-K+ pump as strongly as Na+ ions. These observations indicate that the interactions are bidirectional and mediated by Na+ ions. Also after substitution of extracellular Na+ with Li+, the tail Ih was reduced markedly despite an enhancement of Ih itself, attributable to a negative shift of the reversal potential for I h presumably caused by intracellular accumulation of Li+ ions. This suggests the presence of a microdomain where the interactions can take place. Thus, the bidirectional interactions between Na+-K + pumps and h-channels are likely to be mediated by Na+ microdomain. Consistent with these findings, hyperpolarization-activated and cyclic nucleotide-modulated subunits (HCN1/2) and the Na+-K + pump α3 isoform were colocalized in plasma membrane of mesencephalic trigeminal neurons having numerous spines.","lang":"eng"}],"publist_id":"4257","publication_identifier":{"issn":["0270-6474"],"eissn":["1529-2401"]}},{"type":"journal_article","publication_status":"published","day":"03","publication":"Journal of Neuroscience","title":"Subcellular Localization of Metabotropic GABAB Receptor Subunits GABAB1a/b and GABAB2 in the Rat Hippocampus","year":"2003","_id":"2635","page":"11026 - 11035","language":[{"iso":"eng"}],"publisher":"Society for Neuroscience","external_id":{"pmid":["14657159"]},"volume":23,"citation":{"chicago":"Kulik, Ákos, Imre Vida, Rafael Luján, Carola Haas, Guillermina López Bendito, Ryuichi Shigemoto, and Michael Frotscher. “Subcellular Localization of Metabotropic GABAB Receptor Subunits GABAB1a/b and GABAB2 in the Rat Hippocampus.” Journal of Neuroscience. Society for Neuroscience, 2003. https://doi.org/10.1523/JNEUROSCI.23-35-11026.2003.","ieee":"Á. Kulik et al., “Subcellular Localization of Metabotropic GABAB Receptor Subunits GABAB1a/b and GABAB2 in the Rat Hippocampus,” Journal of Neuroscience, vol. 23, no. 35. Society for Neuroscience, pp. 11026–11035, 2003.","ista":"Kulik Á, Vida I, Luján R, Haas C, López Bendito G, Shigemoto R, Frotscher M. 2003. Subcellular Localization of Metabotropic GABAB Receptor Subunits GABAB1a/b and GABAB2 in the Rat Hippocampus. Journal of Neuroscience. 23(35), 11026–11035.","short":"Á. Kulik, I. Vida, R. Luján, C. Haas, G. López Bendito, R. Shigemoto, M. Frotscher, Journal of Neuroscience 23 (2003) 11026–11035.","ama":"Kulik Á, Vida I, Luján R, et al. Subcellular Localization of Metabotropic GABAB Receptor Subunits GABAB1a/b and GABAB2 in the Rat Hippocampus. Journal of Neuroscience. 2003;23(35):11026-11035. doi:10.1523/JNEUROSCI.23-35-11026.2003","apa":"Kulik, Á., Vida, I., Luján, R., Haas, C., López Bendito, G., Shigemoto, R., & Frotscher, M. (2003). Subcellular Localization of Metabotropic GABAB Receptor Subunits GABAB1a/b and GABAB2 in the Rat Hippocampus. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.23-35-11026.2003","mla":"Kulik, Ákos, et al. “Subcellular Localization of Metabotropic GABAB Receptor Subunits GABAB1a/b and GABAB2 in the Rat Hippocampus.” Journal of Neuroscience, vol. 23, no. 35, Society for Neuroscience, 2003, pp. 11026–35, doi:10.1523/JNEUROSCI.23-35-11026.2003."},"pmid":1,"intvolume":" 23","issue":"35","date_updated":"2026-05-22T09:50:16Z","doi":"10.1523/JNEUROSCI.23-35-11026.2003","publication_identifier":{"issn":["0270-6474"],"eissn":["1529-2401"]},"publist_id":"4263","abstract":[{"lang":"eng","text":"Metabotropic GABAB receptors mediate slow inhibitory effects presynaptically and postsynaptically. Using preembedding immunohistochemical methods combined with quantitative analysis of GABAB receptor subunit immunoreactivity, this study provides a detailed description of the cellular and subcellular localization of GABAB1a/b and GABA B2 in the rat hippocampus. At the light microscopic level, an overlapping distribution of GABAB1a/b and GABAB2 was revealed in the dendritic layers of the hippocampus. In addition, expression of the GABAB1a/b subunit was found in somata of CA1 pyramidal cells and of a subset of GABAergic interneurons. At the electron microscopic level, immunoreactivity for both subunits was observed on presynaptic and, more abundantly, on postsynaptic elements. Presynaptically, subunits were mainly detected in the extrasynaptic membrane and occasionally over the presynaptic membrane specialization of putative glutamatergic and, to a lesser extent, GABAergic axon terminals. Postsynaptically, the majority of GABAB receptor subunits were localized to the extrasynaptic plasma membrane of spines and dendritic shafts of principal cells and shafts of interneuron dendrites. Quantitative analysis revealed enrichment of GABAB1a/b around putative glutamatergic synapses on spines and an even distribution on dendritic shafts of pyramidal cells contacted by GABAergic boutons. The association of GABAB receptors with glutamatergic synapses at both presynaptic and postsynaptic sides indicates their intimate involvement in the modulation of glutamatergic neurotransmission. The dominant extrasynaptic localization of GABAB receptor subunits suggests that their activation is dependent on spillover of GABA requiring simultaneous activity of populations of GABAergic cells as it occurs during population oscillations or epileptic seizures."}],"article_processing_charge":"No","article_type":"original","OA_type":"closed access","quality_controlled":"1","oa_version":"None","month":"12","author":[{"full_name":"Kulik, Ákos","last_name":"Kulik","first_name":"Ákos"},{"first_name":"Imre","last_name":"Vida","full_name":"Vida, Imre"},{"first_name":"Rafael","last_name":"Luján","full_name":"Luján, Rafael"},{"first_name":"Carola","full_name":"Haas, Carola","last_name":"Haas"},{"first_name":"Guillermina","last_name":"López Bendito","full_name":"López Bendito, Guillermina"},{"orcid":"0000-0001-8761-9444","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","last_name":"Shigemoto","full_name":"Shigemoto, Ryuichi","first_name":"Ryuichi"},{"full_name":"Frotscher, Michael","last_name":"Frotscher","first_name":"Michael"}],"scopus_import":"1","date_published":"2003-12-03T00:00:00Z","user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","fulldoi":"https://doi.org/10.1523/JNEUROSCI.23-35-11026.2003","status":"public","extern":"1","date_created":"2018-12-11T11:58:47Z"}]