[{"publisher":"Oxford University Press","language":[{"iso":"eng"}],"page":"2130 - 2140","quality_controlled":"1","title":"Epilepsy-induced motility of differentiated neurons","month":"08","intvolume":"        24","publication_status":"published","oa_version":"None","department":[{"_id":"PeJo"}],"date_created":"2018-12-11T11:56:04Z","author":[{"first_name":"Xuejun","last_name":"Chai","full_name":"Chai, Xuejun"},{"full_name":"Münzner, Gert","last_name":"Münzner","first_name":"Gert"},{"full_name":"Zhao, Shanting","first_name":"Shanting","last_name":"Zhao"},{"first_name":"Stefanie","last_name":"Tinnes","full_name":"Tinnes, Stefanie"},{"id":"3F3CA136-F248-11E8-B48F-1D18A9856A87","last_name":"Kowalski","first_name":"Janina","full_name":"Kowalski, Janina"},{"last_name":"Häussler","first_name":"Ute","full_name":"Häussler, Ute"},{"first_name":"Christina","last_name":"Young","full_name":"Young, Christina"},{"full_name":"Haas, Carola","last_name":"Haas","first_name":"Carola"},{"first_name":"Michael","last_name":"Frotscher","full_name":"Frotscher, Michael"}],"issue":"8","_id":"2164","publication":"Cerebral Cortex","scopus_import":1,"status":"public","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","volume":24,"abstract":[{"lang":"eng","text":"Neuronal ectopia, such as granule cell dispersion (GCD) in temporal lobe epilepsy (TLE), has been assumed to result from a migration defect during development. Indeed, recent studies reported that aberrant migration of neonatal-generated dentate granule cells (GCs) increased the risk to develop epilepsy later in life. On the contrary, in the present study, we show that fully differentiated GCs become motile following the induction of epileptiform activity, resulting in GCD. Hippocampal slice cultures from transgenic mice expressing green fluorescent protein in differentiated, but not in newly generated GCs, were incubated with the glutamate receptor agonist kainate (KA), which induced GC burst activity and GCD. Using real-time microscopy, we observed that KA-exposed, differentiated GCs translocated their cell bodies and changed their dendritic organization. As found in human TLE, KA application was associated with decreased expression of the extracellular matrix protein Reelin, particularly in hilar interneurons. Together these findings suggest that KA-induced motility of differentiated GCs contributes to the development of GCD and establish slice cultures as a model to study neuronal changes induced by epileptiform activity. "}],"publist_id":"4820","doi":"10.1093/cercor/bht067","day":"01","date_published":"2014-08-01T00:00:00Z","type":"journal_article","date_updated":"2021-01-12T06:55:43Z","year":"2014","citation":{"apa":"Chai, X., Münzner, G., Zhao, S., Tinnes, S., Kowalski, J., Häussler, U., … Frotscher, M. (2014). Epilepsy-induced motility of differentiated neurons. <i>Cerebral Cortex</i>. Oxford University Press. <a href=\"https://doi.org/10.1093/cercor/bht067\">https://doi.org/10.1093/cercor/bht067</a>","ama":"Chai X, Münzner G, Zhao S, et al. Epilepsy-induced motility of differentiated neurons. <i>Cerebral Cortex</i>. 2014;24(8):2130-2140. doi:<a href=\"https://doi.org/10.1093/cercor/bht067\">10.1093/cercor/bht067</a>","ieee":"X. Chai <i>et al.</i>, “Epilepsy-induced motility of differentiated neurons,” <i>Cerebral Cortex</i>, vol. 24, no. 8. Oxford University Press, pp. 2130–2140, 2014.","chicago":"Chai, Xuejun, Gert Münzner, Shanting Zhao, Stefanie Tinnes, Janina Kowalski, Ute Häussler, Christina Young, Carola Haas, and Michael Frotscher. “Epilepsy-Induced Motility of Differentiated Neurons.” <i>Cerebral Cortex</i>. Oxford University Press, 2014. <a href=\"https://doi.org/10.1093/cercor/bht067\">https://doi.org/10.1093/cercor/bht067</a>.","short":"X. Chai, G. Münzner, S. Zhao, S. Tinnes, J. Kowalski, U. Häussler, C. Young, C. Haas, M. Frotscher, Cerebral Cortex 24 (2014) 2130–2140.","mla":"Chai, Xuejun, et al. “Epilepsy-Induced Motility of Differentiated Neurons.” <i>Cerebral Cortex</i>, vol. 24, no. 8, Oxford University Press, 2014, pp. 2130–40, doi:<a href=\"https://doi.org/10.1093/cercor/bht067\">10.1093/cercor/bht067</a>.","ista":"Chai X, Münzner G, Zhao S, Tinnes S, Kowalski J, Häussler U, Young C, Haas C, Frotscher M. 2014. Epilepsy-induced motility of differentiated neurons. Cerebral Cortex. 24(8), 2130–2140."}},{"status":"public","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","volume":9,"publist_id":"4807","abstract":[{"lang":"eng","text":"Electron microscopy (EM) allows for the simultaneous visualization of all tissue components at high resolution. However, the extent to which conventional aldehyde fixation and ethanol dehydration of the tissue alter the fine structure of cells and organelles, thereby preventing detection of subtle structural changes induced by an experiment, has remained an issue. Attempts have been made to rapidly freeze tissue to preserve native ultrastructure. Shock-freezing of living tissue under high pressure (high-pressure freezing, HPF) followed by cryosubstitution of the tissue water avoids aldehyde fixation and dehydration in ethanol; the tissue water is immobilized in â ̂1/450 ms, and a close-to-native fine structure of cells, organelles and molecules is preserved. Here we describe a protocol for HPF that is useful to monitor ultrastructural changes associated with functional changes at synapses in the brain but can be applied to many other tissues as well. The procedure requires a high-pressure freezer and takes a minimum of 7 d but can be paused at several points."}],"day":"29","doi":"10.1038/nprot.2014.099","type":"journal_article","date_published":"2014-05-29T00:00:00Z","year":"2014","citation":{"apa":"Studer, D., Zhao, S., Chai, X., Jonas, P. M., Graber, W., Nestel, S., &#38; Frotscher, M. (2014). Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue. <i>Nature Protocols</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/nprot.2014.099\">https://doi.org/10.1038/nprot.2014.099</a>","ama":"Studer D, Zhao S, Chai X, et al. Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue. <i>Nature Protocols</i>. 2014;9(6):1480-1495. doi:<a href=\"https://doi.org/10.1038/nprot.2014.099\">10.1038/nprot.2014.099</a>","chicago":"Studer, Daniel, Shanting Zhao, Xuejun Chai, Peter M Jonas, Werner Graber, Sigrun Nestel, and Michael Frotscher. “Capture of Activity-Induced Ultrastructural Changes at Synapses by High-Pressure Freezing of Brain Tissue.” <i>Nature Protocols</i>. Nature Publishing Group, 2014. <a href=\"https://doi.org/10.1038/nprot.2014.099\">https://doi.org/10.1038/nprot.2014.099</a>.","ieee":"D. Studer <i>et al.</i>, “Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue,” <i>Nature Protocols</i>, vol. 9, no. 6. Nature Publishing Group, pp. 1480–1495, 2014.","mla":"Studer, Daniel, et al. “Capture of Activity-Induced Ultrastructural Changes at Synapses by High-Pressure Freezing of Brain Tissue.” <i>Nature Protocols</i>, vol. 9, no. 6, Nature Publishing Group, 2014, pp. 1480–95, doi:<a href=\"https://doi.org/10.1038/nprot.2014.099\">10.1038/nprot.2014.099</a>.","short":"D. Studer, S. Zhao, X. Chai, P.M. Jonas, W. Graber, S. Nestel, M. Frotscher, Nature Protocols 9 (2014) 1480–1495.","ista":"Studer D, Zhao S, Chai X, Jonas PM, Graber W, Nestel S, Frotscher M. 2014. Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue. Nature Protocols. 9(6), 1480–1495."},"date_updated":"2021-01-12T06:55:47Z","publisher":"Nature Publishing Group","language":[{"iso":"eng"}],"quality_controlled":"1","page":"1480 - 1495","intvolume":"         9","month":"05","title":"Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue","date_created":"2018-12-11T11:56:09Z","department":[{"_id":"PeJo"}],"project":[{"name":"Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen","grant_number":"SFB-TR3-TP10B","_id":"25BDE9A4-B435-11E9-9278-68D0E5697425"}],"oa_version":"None","publication_status":"published","issue":"6","author":[{"first_name":"Daniel","last_name":"Studer","full_name":"Studer, Daniel"},{"last_name":"Zhao","first_name":"Shanting","full_name":"Zhao, Shanting"},{"full_name":"Chai, Xuejun","last_name":"Chai","first_name":"Xuejun"},{"orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M","first_name":"Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Graber","first_name":"Werner","full_name":"Graber, Werner"},{"full_name":"Nestel, Sigrun","first_name":"Sigrun","last_name":"Nestel"},{"full_name":"Frotscher, Michael","last_name":"Frotscher","first_name":"Michael"}],"scopus_import":1,"_id":"2176","publication":"Nature Protocols"},{"ec_funded":1,"quality_controlled":"1","page":"686-693","publisher":"Nature Publishing Group","scopus_import":1,"_id":"2228","issue":"5","author":[{"id":"4AC0145C-F248-11E8-B48F-1D18A9856A87","last_name":"Hu","first_name":"Hua","full_name":"Hu, Hua"},{"first_name":"Peter M","last_name":"Jonas","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"}],"department":[{"_id":"PeJo"}],"date_created":"2018-12-11T11:56:26Z","publication_status":"published","intvolume":"        17","title":"A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons","volume":17,"year":"2014","citation":{"ama":"Hu H, Jonas PM. A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons. <i>Nature Neuroscience</i>. 2014;17(5):686-693. doi:<a href=\"https://doi.org/10.1038/nn.3678\">10.1038/nn.3678</a>","apa":"Hu, H., &#38; Jonas, P. M. (2014). A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons. <i>Nature Neuroscience</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/nn.3678\">https://doi.org/10.1038/nn.3678</a>","ieee":"H. Hu and P. M. Jonas, “A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons,” <i>Nature Neuroscience</i>, vol. 17, no. 5. Nature Publishing Group, pp. 686–693, 2014.","chicago":"Hu, Hua, and Peter M Jonas. “A Supercritical Density of Na^+ Channels Ensures Fast Signaling in GABAergic Interneuron Axons.” <i>Nature Neuroscience</i>. Nature Publishing Group, 2014. <a href=\"https://doi.org/10.1038/nn.3678\">https://doi.org/10.1038/nn.3678</a>.","mla":"Hu, Hua, and Peter M. Jonas. “A Supercritical Density of Na^+ Channels Ensures Fast Signaling in GABAergic Interneuron Axons.” <i>Nature Neuroscience</i>, vol. 17, no. 5, Nature Publishing Group, 2014, pp. 686–93, doi:<a href=\"https://doi.org/10.1038/nn.3678\">10.1038/nn.3678</a>.","short":"H. Hu, P.M. Jonas, Nature Neuroscience 17 (2014) 686–693.","ista":"Hu H, Jonas PM. 2014. A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons. Nature Neuroscience. 17(5), 686–693."},"date_updated":"2021-01-12T06:56:08Z","day":"23","doi":"10.1038/nn.3678","abstract":[{"lang":"eng","text":"Fast-spiking, parvalbumin-expressing GABAergic interneurons, a large proportion of which are basket cells (BCs), have a key role in feedforward and feedback inhibition, gamma oscillations and complex information processing. For these functions, fast propagation of action potentials (APs) from the soma to the presynaptic terminals is important. However, the functional properties of interneuron axons remain elusive. We examined interneuron axons by confocally targeted subcellular patch-clamp recording in rat hippocampal slices. APs were initiated in the proximal axon ∼20 μm from the soma and propagated to the distal axon with high reliability and speed. Subcellular mapping revealed a stepwise increase of Na^+ conductance density from the soma to the proximal axon, followed by a further gradual increase in the distal axon. Active cable modeling and experiments with partial channel block revealed that low axonal Na^+ conductance density was sufficient for reliability, but high Na^+ density was necessary for both speed of propagation and fast-spiking AP phenotype. Our results suggest that a supercritical density of Na^+ channels compensates for the morphological properties of interneuron axons (small segmental diameter, extensive branching and high bouton density), ensuring fast AP propagation and high-frequency repetitive firing."}],"language":[{"iso":"eng"}],"publication":"Nature Neuroscience","project":[{"call_identifier":"FP7","_id":"25C0F108-B435-11E9-9278-68D0E5697425","grant_number":"268548","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons"},{"call_identifier":"FWF","_id":"25C26B1E-B435-11E9-9278-68D0E5697425","name":"Mechanisms of transmitter release at GABAergic synapses","grant_number":"P24909-B24"}],"oa_version":"Submitted Version","month":"03","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4286295/"}],"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","status":"public","type":"journal_article","date_published":"2014-03-23T00:00:00Z","publication_identifier":{"issn":["10976256"]},"oa":1,"publist_id":"4733"},{"oa":1,"publist_id":"4732","publication_identifier":{"issn":["00368075"]},"date_published":"2014-02-01T00:00:00Z","type":"journal_article","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","status":"public","main_file_link":[{"open_access":"1","url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617475/"}],"month":"02","oa_version":"Submitted Version","project":[{"name":"Mechanisms of transmitter release at GABAergic synapses","grant_number":"P24909-B24","_id":"25C26B1E-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"},{"grant_number":"268548","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","call_identifier":"FP7","_id":"25C0F108-B435-11E9-9278-68D0E5697425"}],"publication":"Science","language":[{"iso":"eng"}],"abstract":[{"text":"The distance between Ca^2+ channels and release sensors determines the speed and efficacy of synaptic transmission. Tight &quot;nanodomain&quot; channel-sensor coupling initiates transmitter release at synapses in the mature brain, whereas loose &quot;microdomain&quot; coupling appears restricted to early developmental stages. To probe the coupling configuration at a plastic synapse in the mature central nervous system, we performed paired recordings between mossy fiber terminals and CA3 pyramidal neurons in rat hippocampus. Millimolar concentrations of both the fast Ca^2+ chelator BAPTA [1,2-bis(2-aminophenoxy)ethane- N,N, N′,N′-tetraacetic acid] and the slow chelator EGTA efficiently suppressed transmitter release, indicating loose coupling between Ca^2+ channels and release sensors. Loose coupling enabled the control of initial release probability by fast endogenous Ca^2+ buffers and the generation of facilitation by buffer saturation. Thus, loose coupling provides the molecular framework for presynaptic plasticity.","lang":"eng"}],"doi":"10.1126/science.1244811","day":"01","date_updated":"2021-01-12T06:56:09Z","year":"2014","citation":{"chicago":"Vyleta, Nicholas, and Peter M Jonas. “Loose Coupling between Ca^2+ Channels and Release Sensors at a Plastic Hippocampal Synapse.” <i>Science</i>. American Association for the Advancement of Science, 2014. <a href=\"https://doi.org/10.1126/science.1244811\">https://doi.org/10.1126/science.1244811</a>.","ieee":"N. Vyleta and P. M. Jonas, “Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse,” <i>Science</i>, vol. 343, no. 6171. American Association for the Advancement of Science, pp. 665–670, 2014.","ama":"Vyleta N, Jonas PM. Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse. <i>Science</i>. 2014;343(6171):665-670. doi:<a href=\"https://doi.org/10.1126/science.1244811\">10.1126/science.1244811</a>","apa":"Vyleta, N., &#38; Jonas, P. M. (2014). Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse. <i>Science</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/science.1244811\">https://doi.org/10.1126/science.1244811</a>","ista":"Vyleta N, Jonas PM. 2014. Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse. Science. 343(6171), 665–670.","mla":"Vyleta, Nicholas, and Peter M. Jonas. “Loose Coupling between Ca^2+ Channels and Release Sensors at a Plastic Hippocampal Synapse.” <i>Science</i>, vol. 343, no. 6171, American Association for the Advancement of Science, 2014, pp. 665–70, doi:<a href=\"https://doi.org/10.1126/science.1244811\">10.1126/science.1244811</a>.","short":"N. Vyleta, P.M. Jonas, Science 343 (2014) 665–670."},"volume":343,"title":"Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse","intvolume":"       343","publication_status":"published","department":[{"_id":"PeJo"}],"date_created":"2018-12-11T11:56:27Z","author":[{"id":"36C4978E-F248-11E8-B48F-1D18A9856A87","full_name":"Vyleta, Nicholas","first_name":"Nicholas","last_name":"Vyleta"},{"id":"353C1B58-F248-11E8-B48F-1D18A9856A87","first_name":"Peter M","last_name":"Jonas","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M"}],"issue":"6171","_id":"2229","scopus_import":1,"publisher":"American Association for the Advancement of Science","page":"665 - 670","quality_controlled":"1","ec_funded":1},{"publisher":"Frontiers Research Foundation","file_date_updated":"2020-07-14T12:45:34Z","quality_controlled":"1","title":"Stimfit: Quantifying electrophysiological data with Python","pubrep_id":"425","intvolume":"         8","publication_status":"published","department":[{"_id":"ScienComp"},{"_id":"PeJo"}],"date_created":"2018-12-11T11:56:27Z","author":[{"id":"30CC5506-F248-11E8-B48F-1D18A9856A87","full_name":"Guzmán, José","last_name":"Guzmán","first_name":"José"},{"id":"45BF87EE-F248-11E8-B48F-1D18A9856A87","last_name":"Schlögl","first_name":"Alois","full_name":"Schlögl, Alois","orcid":"0000-0002-5621-8100"},{"first_name":"Christoph","last_name":"Schmidt Hieber","full_name":"Schmidt Hieber, Christoph"}],"issue":"FEB","_id":"2230","scopus_import":1,"ddc":["570"],"volume":8,"abstract":[{"text":"Intracellular electrophysiological recordings provide crucial insights into elementary neuronal signals such as action potentials and synaptic currents. Analyzing and interpreting these signals is essential for a quantitative understanding of neuronal information processing, and requires both fast data visualization and ready access to complex analysis routines. To achieve this goal, we have developed Stimfit, a free software package for cellular neurophysiology with a Python scripting interface and a built-in Python shell. The program supports most standard file formats for cellular neurophysiology and other biomedical signals through the Biosig library. To quantify and interpret the activity of single neurons and communication between neurons, the program includes algorithms to characterize the kinetics of presynaptic action potentials and postsynaptic currents, estimate latencies between pre- and postsynaptic events, and detect spontaneously occurring events. We validate and benchmark these algorithms, give estimation errors, and provide sample use cases, showing that Stimfit represents an efficient, accessible and extensible way to accurately analyze and interpret neuronal signals.","lang":"eng"}],"doi":"10.3389/fninf.2014.00016","day":"21","date_updated":"2021-01-12T06:56:09Z","citation":{"short":"J. Guzmán, A. Schlögl, C. Schmidt Hieber, Frontiers in Neuroinformatics 8 (2014).","mla":"Guzmán, José, et al. “Stimfit: Quantifying Electrophysiological Data with Python.” <i>Frontiers in Neuroinformatics</i>, vol. 8, no. FEB, 16, Frontiers Research Foundation, 2014, doi:<a href=\"https://doi.org/10.3389/fninf.2014.00016\">10.3389/fninf.2014.00016</a>.","ista":"Guzmán J, Schlögl A, Schmidt Hieber C. 2014. Stimfit: Quantifying electrophysiological data with Python. Frontiers in Neuroinformatics. 8(FEB), 16.","apa":"Guzmán, J., Schlögl, A., &#38; Schmidt Hieber, C. (2014). Stimfit: Quantifying electrophysiological data with Python. <i>Frontiers in Neuroinformatics</i>. Frontiers Research Foundation. <a href=\"https://doi.org/10.3389/fninf.2014.00016\">https://doi.org/10.3389/fninf.2014.00016</a>","ama":"Guzmán J, Schlögl A, Schmidt Hieber C. Stimfit: Quantifying electrophysiological data with Python. <i>Frontiers in Neuroinformatics</i>. 2014;8(FEB). doi:<a href=\"https://doi.org/10.3389/fninf.2014.00016\">10.3389/fninf.2014.00016</a>","chicago":"Guzmán, José, Alois Schlögl, and Christoph Schmidt Hieber. “Stimfit: Quantifying Electrophysiological Data with Python.” <i>Frontiers in Neuroinformatics</i>. Frontiers Research Foundation, 2014. <a href=\"https://doi.org/10.3389/fninf.2014.00016\">https://doi.org/10.3389/fninf.2014.00016</a>.","ieee":"J. Guzmán, A. Schlögl, and C. Schmidt Hieber, “Stimfit: Quantifying electrophysiological data with Python,” <i>Frontiers in Neuroinformatics</i>, vol. 8, no. FEB. Frontiers Research Foundation, 2014."},"year":"2014","language":[{"iso":"eng"}],"month":"02","article_number":"16","oa_version":"Published Version","publication":"Frontiers in Neuroinformatics","has_accepted_license":"1","status":"public","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","file":[{"relation":"main_file","access_level":"open_access","creator":"system","file_id":"4935","checksum":"eeca00bba7232ff7d27db83321f6ea30","file_size":2883372,"date_created":"2018-12-12T10:12:17Z","file_name":"IST-2016-425-v1+1_fninf-08-00016.pdf","content_type":"application/pdf","date_updated":"2020-07-14T12:45:34Z"}],"publist_id":"4731","oa":1,"publication_identifier":{"issn":["16625196"]},"date_published":"2014-02-21T00:00:00Z","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"}},{"file":[{"content_type":"application/pdf","file_name":"IST-2016-422-v1+1_1-s2.0-S0896627313009227-main.pdf","date_updated":"2020-07-14T12:45:35Z","checksum":"438547cfcd9045a22f065f2019f07849","file_size":4373072,"date_created":"2018-12-12T10:09:48Z","creator":"system","file_id":"4773","access_level":"open_access","relation":"main_file"}],"status":"public","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_identifier":{"issn":["08966273"]},"oa":1,"publist_id":"4692","type":"journal_article","date_published":"2014-01-08T00:00:00Z","language":[{"iso":"eng"}],"project":[{"call_identifier":"FP7","_id":"25C0F108-B435-11E9-9278-68D0E5697425","grant_number":"268548","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons"},{"name":"Mechanisms of transmitter release at GABAergic synapses","grant_number":"P24909-B24","call_identifier":"FWF","_id":"25C26B1E-B435-11E9-9278-68D0E5697425"}],"oa_version":"Published Version","month":"01","has_accepted_license":"1","publication":"Neuron","volume":81,"ddc":["570"],"day":"08","doi":"10.1016/j.neuron.2013.09.046","abstract":[{"text":"Theta-gamma network oscillations are thought to represent key reference signals for information processing in neuronal ensembles, but the underlying synaptic mechanisms remain unclear. To address this question, we performed whole-cell (WC) patch-clamp recordings from mature hippocampal granule cells (GCs) in vivo in the dentate gyrus of anesthetized and awake rats. GCs in vivo fired action potentials at low frequency, consistent with sparse coding in the dentate gyrus. GCs were exposed to barrages of fast AMPAR-mediated excitatory postsynaptic currents (EPSCs), primarily relayed from the entorhinal cortex, and inhibitory postsynaptic currents (IPSCs), presumably generated by local interneurons. EPSCs exhibited coherence with the field potential predominantly in the theta frequency band, whereas IPSCs showed coherence primarily in the gamma range. Action potentials in GCs were phase locked to network oscillations. Thus, theta-gamma-modulated synaptic currents may provide a framework for sparse temporal coding of information in the dentate gyrus.","lang":"eng"}],"citation":{"short":"A. Pernia-Andrade, P.M. Jonas, Neuron 81 (2014) 140–152.","mla":"Pernia-Andrade, Alejandro, and Peter M. Jonas. “Theta-Gamma-Modulated Synaptic Currents in Hippocampal Granule Cells in Vivo Define a Mechanism for Network Oscillations.” <i>Neuron</i>, vol. 81, no. 1, Elsevier, 2014, pp. 140–52, doi:<a href=\"https://doi.org/10.1016/j.neuron.2013.09.046\">10.1016/j.neuron.2013.09.046</a>.","ista":"Pernia-Andrade A, Jonas PM. 2014. Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations. Neuron. 81(1), 140–152.","apa":"Pernia-Andrade, A., &#38; Jonas, P. M. (2014). Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations. <i>Neuron</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuron.2013.09.046\">https://doi.org/10.1016/j.neuron.2013.09.046</a>","ama":"Pernia-Andrade A, Jonas PM. Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations. <i>Neuron</i>. 2014;81(1):140-152. doi:<a href=\"https://doi.org/10.1016/j.neuron.2013.09.046\">10.1016/j.neuron.2013.09.046</a>","ieee":"A. Pernia-Andrade and P. M. Jonas, “Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations,” <i>Neuron</i>, vol. 81, no. 1. Elsevier, pp. 140–152, 2014.","chicago":"Pernia-Andrade, Alejandro, and Peter M Jonas. “Theta-Gamma-Modulated Synaptic Currents in Hippocampal Granule Cells in Vivo Define a Mechanism for Network Oscillations.” <i>Neuron</i>. Elsevier, 2014. <a href=\"https://doi.org/10.1016/j.neuron.2013.09.046\">https://doi.org/10.1016/j.neuron.2013.09.046</a>."},"year":"2014","date_updated":"2021-01-12T06:56:19Z","publisher":"Elsevier","quality_controlled":"1","ec_funded":1,"page":"140 - 152","file_date_updated":"2020-07-14T12:45:35Z","department":[{"_id":"PeJo"}],"date_created":"2018-12-11T11:56:35Z","publication_status":"published","intvolume":"        81","title":"Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations","pubrep_id":"422","scopus_import":1,"_id":"2254","issue":"1","author":[{"full_name":"Pernia-Andrade, Alejandro","first_name":"Alejandro","last_name":"Pernia-Andrade","id":"36963E98-F248-11E8-B48F-1D18A9856A87"},{"id":"353C1B58-F248-11E8-B48F-1D18A9856A87","full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804","last_name":"Jonas","first_name":"Peter M"}]},{"doi":"10.1002/hipo.22214","day":"01","abstract":[{"lang":"eng","text":"GABAergic inhibitory interneurons control fundamental aspects of neuronal network function. Their functional roles are assumed to be defined by the identity of their input synapses, the architecture of their dendritic tree, the passive and active membrane properties and finally the nature of their postsynaptic targets. Indeed, interneurons display a high degree of morphological and physiological heterogeneity. However, whether their morphological and physiological characteristics are correlated and whether interneuron diversity can be described by a continuum of GABAergic cell types or by distinct classes has remained unclear. Here we perform a detailed morphological and physiological characterization of GABAergic cells in the dentate gyrus, the input region of the hippocampus. To achieve an unbiased and efficient sampling and classification we used knock-in mice expressing the enhanced green fluorescent protein (eGFP) in glutamate decarboxylase 67 (GAD67)-positive neurons and performed cluster analysis. We identified five interneuron classes, each of them characterized by a distinct set of anatomical and physiological parameters. Cross-correlation analysis further revealed a direct relation between morphological and physiological properties indicating that dentate gyrus interneurons fall into functionally distinct classes which may differentially control neuronal network activity."}],"date_updated":"2021-01-12T06:56:32Z","year":"2014","citation":{"ieee":"J. Hosp <i>et al.</i>, “Morpho-physiological criteria divide dentate gyrus interneurons into classes,” <i>Hippocampus</i>, vol. 23, no. 2. Wiley-Blackwell, pp. 189–203, 2014.","chicago":"Hosp, Jonas, Michael Strüber, Yuchio Yanagawa, Kunihiko Obata, Imre Vida, Peter M Jonas, and Marlene Bartos. “Morpho-Physiological Criteria Divide Dentate Gyrus Interneurons into Classes.” <i>Hippocampus</i>. Wiley-Blackwell, 2014. <a href=\"https://doi.org/10.1002/hipo.22214\">https://doi.org/10.1002/hipo.22214</a>.","ama":"Hosp J, Strüber M, Yanagawa Y, et al. Morpho-physiological criteria divide dentate gyrus interneurons into classes. <i>Hippocampus</i>. 2014;23(2):189-203. doi:<a href=\"https://doi.org/10.1002/hipo.22214\">10.1002/hipo.22214</a>","apa":"Hosp, J., Strüber, M., Yanagawa, Y., Obata, K., Vida, I., Jonas, P. M., &#38; Bartos, M. (2014). Morpho-physiological criteria divide dentate gyrus interneurons into classes. <i>Hippocampus</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1002/hipo.22214\">https://doi.org/10.1002/hipo.22214</a>","ista":"Hosp J, Strüber M, Yanagawa Y, Obata K, Vida I, Jonas PM, Bartos M. 2014. Morpho-physiological criteria divide dentate gyrus interneurons into classes. Hippocampus. 23(2), 189–203.","short":"J. Hosp, M. Strüber, Y. Yanagawa, K. Obata, I. Vida, P.M. Jonas, M. Bartos, Hippocampus 23 (2014) 189–203.","mla":"Hosp, Jonas, et al. “Morpho-Physiological Criteria Divide Dentate Gyrus Interneurons into Classes.” <i>Hippocampus</i>, vol. 23, no. 2, Wiley-Blackwell, 2014, pp. 189–203, doi:<a href=\"https://doi.org/10.1002/hipo.22214\">10.1002/hipo.22214</a>."},"volume":23,"acknowledgement":"Funded by Deutsche Forschungsgemeinschaft. Grant Numbers: SFB 505, SFB 780, BA1582/2-1 Excellence Initiative of the German Research Foundation (Spemann Graduate School). Grant Number: GSC-4 Lichtenberg Professorship-Award (VW-Foundation); Schram-Foundation; Excellence Initiative Brain Links-Brain Tools. The authors thank Drs. Jonas-Frederic Sauer and Claudio Elgueta for critically reading the manuscript. They also thank Karin Winterhalter, Margit Northemann and Ulrich Nöller for technical assistance.","ddc":["570"],"publication_status":"published","date_created":"2018-12-11T11:56:46Z","department":[{"_id":"PeJo"}],"title":"Morpho-physiological criteria divide dentate gyrus interneurons into classes","pubrep_id":"461","intvolume":"        23","_id":"2285","scopus_import":1,"license":"https://creativecommons.org/licenses/by-nc/4.0/","author":[{"first_name":"Jonas","last_name":"Hosp","full_name":"Hosp, Jonas"},{"last_name":"Strüber","first_name":"Michael","full_name":"Strüber, Michael"},{"last_name":"Yanagawa","first_name":"Yuchio","full_name":"Yanagawa, Yuchio"},{"full_name":"Obata, Kunihiko","first_name":"Kunihiko","last_name":"Obata"},{"last_name":"Vida","first_name":"Imre","full_name":"Vida, Imre"},{"id":"353C1B58-F248-11E8-B48F-1D18A9856A87","full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804","last_name":"Jonas","first_name":"Peter M"},{"full_name":"Bartos, Marlene","first_name":"Marlene","last_name":"Bartos"}],"issue":"2","publisher":"Wiley-Blackwell","page":"189 - 203","quality_controlled":"1","file_date_updated":"2020-07-14T12:45:37Z","oa":1,"publist_id":"4646","tmp":{"name":"Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)","image":"/images/cc_by_nc.png","short":"CC BY-NC (4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc/4.0/legalcode"},"date_published":"2014-02-01T00:00:00Z","type":"journal_article","file":[{"file_name":"IST-2016-461-v1+1_Hosp_et_al-2014-Hippocampus.pdf","content_type":"application/pdf","date_updated":"2020-07-14T12:45:37Z","file_size":801589,"checksum":"ff6bc75a79dbc985a2e31b79253e6444","date_created":"2018-12-12T10:15:54Z","creator":"system","file_id":"5178","access_level":"open_access","relation":"main_file"}],"status":"public","user_id":"3FFCCD3A-F248-11E8-B48F-1D18A9856A87","oa_version":"Published Version","month":"02","publication":"Hippocampus","has_accepted_license":"1","language":[{"iso":"eng"}]},{"oa_version":"Submitted Version","article_number":"000010151520134181","month":"08","has_accepted_license":"1","publication":"Biomedical Engineering / Biomedizinische Technik","conference":{"end_date":"2013-09-21","location":"Graz, Austria","start_date":"2013-09-19","name":"BMT: Biomedizinische Technik "},"keyword":["biomedical engineering","data analysis","free software"],"language":[{"iso":"eng"}],"publication_identifier":{"eissn":["1862-278X"],"issn":["0013-5585"]},"oa":1,"type":"journal_article","date_published":"2013-08-01T00:00:00Z","file":[{"file_name":"Schloegl_Abstract-BMT2013.pdf","content_type":"application/pdf","date_updated":"2021-12-01T14:38:08Z","checksum":"cdfc5339b530a25d6079f7223f0b1f16","file_size":149825,"date_created":"2021-12-01T14:38:08Z","creator":"schloegl","file_id":"10397","access_level":"open_access","success":1,"relation":"main_file"}],"status":"public","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","article_processing_charge":"No","date_created":"2021-12-01T14:35:35Z","department":[{"_id":"PeJo"}],"publication_status":"published","intvolume":"        58","title":"Stimfit: A fast visualization and analysis environment for cellular neurophysiology","pmid":1,"_id":"10396","issue":"SI-1-Track-G","author":[{"first_name":"Alois","last_name":"Schlögl","orcid":"0000-0002-5621-8100","full_name":"Schlögl, Alois","id":"45BF87EE-F248-11E8-B48F-1D18A9856A87"},{"id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M","first_name":"Peter M","last_name":"Jonas"},{"first_name":"C.","last_name":"Schmidt-Hieber","full_name":"Schmidt-Hieber, C."},{"last_name":"Guzman","first_name":"S. J.","full_name":"Guzman, S. J."}],"publisher":"De Gruyter","article_type":"original","quality_controlled":"1","file_date_updated":"2021-12-01T14:38:08Z","day":"01","doi":"10.1515/bmt-2013-4181","abstract":[{"lang":"eng","text":"Stimfit is a free cross-platform software package for viewing and analyzing electrophysiological data. It supports most standard file types for cellular neurophysiology and other biomedical formats. Its analysis algorithms have been used and validated in several experimental laboratories. Its embedded Python scripting interface makes Stimfit highly extensible and customizable."}],"year":"2013","citation":{"ama":"Schlögl A, Jonas PM, Schmidt-Hieber C, Guzman SJ. Stimfit: A fast visualization and analysis environment for cellular neurophysiology. <i>Biomedical Engineering / Biomedizinische Technik</i>. 2013;58(SI-1-Track-G). doi:<a href=\"https://doi.org/10.1515/bmt-2013-4181\">10.1515/bmt-2013-4181</a>","apa":"Schlögl, A., Jonas, P. M., Schmidt-Hieber, C., &#38; Guzman, S. J. (2013). Stimfit: A fast visualization and analysis environment for cellular neurophysiology. <i>Biomedical Engineering / Biomedizinische Technik</i>. Graz, Austria: De Gruyter. <a href=\"https://doi.org/10.1515/bmt-2013-4181\">https://doi.org/10.1515/bmt-2013-4181</a>","ieee":"A. Schlögl, P. M. Jonas, C. Schmidt-Hieber, and S. J. Guzman, “Stimfit: A fast visualization and analysis environment for cellular neurophysiology,” <i>Biomedical Engineering / Biomedizinische Technik</i>, vol. 58, no. SI-1-Track-G. De Gruyter, 2013.","chicago":"Schlögl, Alois, Peter M Jonas, C. Schmidt-Hieber, and S. J. Guzman. “Stimfit: A Fast Visualization and Analysis Environment for Cellular Neurophysiology.” <i>Biomedical Engineering / Biomedizinische Technik</i>. De Gruyter, 2013. <a href=\"https://doi.org/10.1515/bmt-2013-4181\">https://doi.org/10.1515/bmt-2013-4181</a>.","short":"A. Schlögl, P.M. Jonas, C. Schmidt-Hieber, S.J. Guzman, Biomedical Engineering / Biomedizinische Technik 58 (2013).","mla":"Schlögl, Alois, et al. “Stimfit: A Fast Visualization and Analysis Environment for Cellular Neurophysiology.” <i>Biomedical Engineering / Biomedizinische Technik</i>, vol. 58, no. SI-1-Track-G, 000010151520134181, De Gruyter, 2013, doi:<a href=\"https://doi.org/10.1515/bmt-2013-4181\">10.1515/bmt-2013-4181</a>.","ista":"Schlögl A, Jonas PM, Schmidt-Hieber C, Guzman SJ. 2013. Stimfit: A fast visualization and analysis environment for cellular neurophysiology. Biomedical Engineering / Biomedizinische Technik. 58(SI-1-Track-G), 000010151520134181."},"date_updated":"2021-12-02T12:51:12Z","external_id":{"pmid":["24042795"]},"volume":58,"ddc":["005","610"]},{"abstract":[{"text":"Spontaneous postsynaptic currents (PSCs) provide key information about the mechanisms of synaptic transmission and the activity modes of neuronal networks. However, detecting spontaneous PSCs in vitro and in vivo has been challenging, because of the small amplitude, the variable kinetics, and the undefined time of generation of these events. Here, we describe a, to our knowledge, new method for detecting spontaneous synaptic events by deconvolution, using a template that approximates the average time course of spontaneous PSCs. A recorded PSC trace is deconvolved from the template, resulting in a series of delta-like functions. The maxima of these delta-like events are reliably detected, revealing the precise onset times of the spontaneous PSCs. Among all detection methods, the deconvolution-based method has a unique temporal resolution, allowing the detection of individual events in high-frequency bursts. Furthermore, the deconvolution-based method has a high amplitude resolution, because deconvolution can substantially increase the signal/noise ratio. When tested against previously published methods using experimental data, the deconvolution-based method was superior for spontaneous PSCs recorded in vivo. Using the high-resolution deconvolution-based detection algorithm, we show that the frequency of spontaneous excitatory postsynaptic currents in dentate gyrus granule cells is 4.5 times higher in vivo than in vitro.","lang":"eng"}],"doi":"10.1016/j.bpj.2012.08.039","day":"03","external_id":{"pmid":["23062335"]},"date_updated":"2021-01-12T07:40:01Z","year":"2012","citation":{"ista":"Pernia-Andrade A, Goswami S, Stickler Y, Fröbe U, Schlögl A, Jonas PM. 2012. A deconvolution based method with high sensitivity and temporal resolution for detection of spontaneous synaptic currents in vitro and in vivo. Biophysical Journal. 103(7), 1429–1439.","mla":"Pernia-Andrade, Alejandro, et al. “A Deconvolution Based Method with High Sensitivity and Temporal Resolution for Detection of Spontaneous Synaptic Currents in Vitro and in Vivo.” <i>Biophysical Journal</i>, vol. 103, no. 7, Biophysical, 2012, pp. 1429–39, doi:<a href=\"https://doi.org/10.1016/j.bpj.2012.08.039\">10.1016/j.bpj.2012.08.039</a>.","short":"A. Pernia-Andrade, S. Goswami, Y. Stickler, U. Fröbe, A. Schlögl, P.M. Jonas, Biophysical Journal 103 (2012) 1429–1439.","ieee":"A. Pernia-Andrade, S. Goswami, Y. Stickler, U. Fröbe, A. Schlögl, and P. M. Jonas, “A deconvolution based method with high sensitivity and temporal resolution for detection of spontaneous synaptic currents in vitro and in vivo,” <i>Biophysical Journal</i>, vol. 103, no. 7. Biophysical, pp. 1429–1439, 2012.","chicago":"Pernia-Andrade, Alejandro, Sarit Goswami, Yvonne Stickler, Ulrich Fröbe, Alois Schlögl, and Peter M Jonas. “A Deconvolution Based Method with High Sensitivity and Temporal Resolution for Detection of Spontaneous Synaptic Currents in Vitro and in Vivo.” <i>Biophysical Journal</i>. Biophysical, 2012. <a href=\"https://doi.org/10.1016/j.bpj.2012.08.039\">https://doi.org/10.1016/j.bpj.2012.08.039</a>.","ama":"Pernia-Andrade A, Goswami S, Stickler Y, Fröbe U, Schlögl A, Jonas PM. A deconvolution based method with high sensitivity and temporal resolution for detection of spontaneous synaptic currents in vitro and in vivo. <i>Biophysical Journal</i>. 2012;103(7):1429-1439. doi:<a href=\"https://doi.org/10.1016/j.bpj.2012.08.039\">10.1016/j.bpj.2012.08.039</a>","apa":"Pernia-Andrade, A., Goswami, S., Stickler, Y., Fröbe, U., Schlögl, A., &#38; Jonas, P. M. (2012). A deconvolution based method with high sensitivity and temporal resolution for detection of spontaneous synaptic currents in vitro and in vivo. <i>Biophysical Journal</i>. Biophysical. <a href=\"https://doi.org/10.1016/j.bpj.2012.08.039\">https://doi.org/10.1016/j.bpj.2012.08.039</a>"},"acknowledgement":"This work was supported by the Deutsche Forschungsgemeinschaft (TR3/B10) and a European Research Council Advanced grant to P.J.\r\nWe thank H. Hu, S. J. Guzman, and C. Schmidt-Hieber for critically reading the manuscript, I. Koeva and F. Marr for technical support, and E. Kramberger for editorial assistance.\r\n","volume":103,"title":"A deconvolution based method with high sensitivity and temporal resolution for detection of spontaneous synaptic currents in vitro and in vivo","intvolume":"       103","publication_status":"published","department":[{"_id":"PeJo"},{"_id":"ScienComp"}],"date_created":"2018-12-11T12:00:32Z","author":[{"id":"36963E98-F248-11E8-B48F-1D18A9856A87","last_name":"Pernia-Andrade","first_name":"Alejandro","full_name":"Pernia-Andrade, Alejandro"},{"last_name":"Goswami","first_name":"Sarit","full_name":"Goswami, Sarit","id":"3A578F32-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Stickler, Yvonne","last_name":"Stickler","first_name":"Yvonne","id":"63B76600-E9CC-11E9-9B5F-82450873F7A1"},{"full_name":"Fröbe, Ulrich","last_name":"Fröbe","first_name":"Ulrich"},{"id":"45BF87EE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-5621-8100","full_name":"Schlögl, Alois","first_name":"Alois","last_name":"Schlögl"},{"first_name":"Peter M","last_name":"Jonas","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"}],"issue":"7","pmid":1,"_id":"2954","scopus_import":1,"publisher":"Biophysical","page":"1429 - 1439","quality_controlled":"1","publist_id":"3774","oa":1,"date_published":"2012-10-03T00:00:00Z","type":"journal_article","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","status":"public","main_file_link":[{"url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3471482/","open_access":"1"}],"month":"10","oa_version":"Submitted Version","project":[{"_id":"25BDE9A4-B435-11E9-9278-68D0E5697425","name":"Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen","grant_number":"SFB-TR3-TP10B"}],"publication":"Biophysical Journal","language":[{"iso":"eng"}]},{"status":"public","related_material":{"record":[{"relation":"part_of_dissertation","id":"3258","status":"public"}]},"user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","degree_awarded":"PhD","publication_identifier":{"issn":["2663-337X"]},"day":"01","supervisor":[{"id":"353C1B58-F248-11E8-B48F-1D18A9856A87","full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804","last_name":"Jonas","first_name":"Peter M"}],"abstract":[{"lang":"eng","text":"CA3 pyramidal neurons are important for memory formation and pattern completion in the hippocampal network. These neurons receive multiple excitatory inputs from numerous sources. Therefore, the rules of spatiotemporal integration of multiple synaptic inputs and propagation of action potentials are important to understand how CA3 neurons contribute to higher brain functions at cellular level. By using confocally targeted patch-clamp recording techniques, we investigated the biophysical properties of rat CA3 pyramidal neuron dendrites. We found two distinct dendritic domains critical for action potential initiation and propagation: In the proximal domain, action potentials initiated in the axon backpropagate actively with large amplitude and fast time course. In the distal domain, Na+-channel mediated dendritic spikes are efficiently evoked by local dendritic depolarization or waveforms mimicking synaptic events. These findings can be explained by a high Na+-to-K+ conductance density ratio of CA3 pyramidal neuron dendrites. The results challenge the prevailing view that proximal mossy fiber inputs activate CA3 pyramidal neurons more efficiently than distal perforant inputs by showing that the distal synapses trigger a different form of activity represented by dendritic spikes. The high probability of dendritic spike initiation in the distal area may enhance the computational power of CA3 pyramidal neurons in the hippocampal network.  "}],"publist_id":"3755","date_updated":"2023-09-07T11:43:51Z","citation":{"short":"S. Kim, Active Properties of Hippocampal CA3 Pyramidal Neuron Dendrites, Institute of Science and Technology Austria, 2012.","mla":"Kim, Sooyun. <i>Active Properties of Hippocampal CA3 Pyramidal Neuron Dendrites</i>. Institute of Science and Technology Austria, 2012.","ista":"Kim S. 2012. Active properties of hippocampal CA3 pyramidal neuron dendrites. Institute of Science and Technology Austria.","ama":"Kim S. Active properties of hippocampal CA3 pyramidal neuron dendrites. 2012.","apa":"Kim, S. (2012). <i>Active properties of hippocampal CA3 pyramidal neuron dendrites</i>. Institute of Science and Technology Austria.","ieee":"S. Kim, “Active properties of hippocampal CA3 pyramidal neuron dendrites,” Institute of Science and Technology Austria, 2012.","chicago":"Kim, Sooyun. “Active Properties of Hippocampal CA3 Pyramidal Neuron Dendrites.” Institute of Science and Technology Austria, 2012."},"year":"2012","date_published":"2012-06-01T00:00:00Z","type":"dissertation","publisher":"Institute of Science and Technology Austria","page":"65","language":[{"iso":"eng"}],"oa_version":"None","publication_status":"published","department":[{"_id":"PeJo"},{"_id":"GradSch"}],"article_processing_charge":"No","date_created":"2018-12-11T12:00:35Z","month":"06","title":"Active properties of hippocampal CA3 pyramidal neuron dendrites","alternative_title":["ISTA Thesis"],"_id":"2964","author":[{"last_name":"Kim","first_name":"Sooyun","full_name":"Kim, Sooyun","id":"394AB1C8-F248-11E8-B48F-1D18A9856A87"}]},{"publisher":"Society for Neuroscience","page":"14294 - 14304","quality_controlled":"1","publication_status":"published","date_created":"2018-12-11T12:00:36Z","department":[{"_id":"PeJo"}],"title":"Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling","intvolume":"        32","pmid":1,"_id":"2969","scopus_import":1,"author":[{"id":"3A578F32-F248-11E8-B48F-1D18A9856A87","full_name":"Goswami, Sarit","first_name":"Sarit","last_name":"Goswami"},{"full_name":"Bucurenciu, Iancu","first_name":"Iancu","last_name":"Bucurenciu"},{"id":"353C1B58-F248-11E8-B48F-1D18A9856A87","last_name":"Jonas","first_name":"Peter M","full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804"}],"issue":"41","acknowledgement":"This work was supported by grants from the Deutsche Forschungsgemeinschaft (TR 3/B10, Leibniz program, GSC-4 Spemann Graduate School) and the European Union (European Research Council Advanced Grant).","volume":32,"doi":"10.1523/JNEUROSCI.6104-11.2012","day":"10","abstract":[{"text":"The coupling between presynaptic Ca^(2+) channels and Ca^(2+) sensors of exocytosis is a key determinant of synaptic transmission. Evoked release from parvalbumin (PV)-expressing interneurons is triggered by nanodomain coupling of P/Q-type Ca^(2+) channels, whereas release from cholecystokinin (CCK)-containing interneurons is generated by microdomain coupling of N-type channels. Nanodomain coupling has several functional advantages, including speed and efficacy of transmission. One potential disadvantage is that stochastic\r\nopening of presynaptic Ca^(2+) channels may trigger spontaneous transmitter release. We addressed this possibility in rat hippocampal\r\ngranule cells, which receive converging inputs from different inhibitory sources. Both reduction of extracellular Ca^(2+) concentration and the unselective Ca^(2+) channel blocker Cd^(2+) reduced the frequency of miniature IPSCs (mIPSCs) in granule cells by ~50%, suggesting that the opening of presynaptic Ca^(2+) channels contributes to spontaneous release. Application of the selective P/Q-type Ca^(2+) channel blocker\r\nω-agatoxin IVa had no detectable effects, whereas both the N-type blocker ω-conotoxin GVIa and the L-type blocker nimodipine reduced\r\nmIPSC frequency. Furthermore, both the fast Ca^(2+) chelator BAPTA-AM and the slow chelator EGTA-AM reduced the mIPSC frequency,\r\nsuggesting that Ca^(2+)-dependent spontaneous release is triggered by microdomain rather than nanodomain coupling. The CB_(1) receptor\r\nagonist WIN 55212-2 also decreased spontaneous release; this effect was occluded by prior application of ω-conotoxin GVIa, suggesting that a major fraction of Ca^(2+)-dependent spontaneous release was generated at the terminals of CCK-expressing interneurons. Tonic inhibition generated by spontaneous opening of presynaptic N- and L-type Ca^(2+) channels may be important for hippocampal information processing.\r\n","lang":"eng"}],"date_updated":"2021-01-12T07:40:08Z","year":"2012","citation":{"ama":"Goswami S, Bucurenciu I, Jonas PM. Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling. <i>Journal of Neuroscience</i>. 2012;32(41):14294-14304. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.6104-11.2012\">10.1523/JNEUROSCI.6104-11.2012</a>","apa":"Goswami, S., Bucurenciu, I., &#38; Jonas, P. M. (2012). Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.6104-11.2012\">https://doi.org/10.1523/JNEUROSCI.6104-11.2012</a>","chicago":"Goswami, Sarit, Iancu Bucurenciu, and Peter M Jonas. “Miniature IPSCs in Hippocampal Granule Cells Are Triggered by Voltage-Gated Ca^(2+) Channels via Microdomain Coupling.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2012. <a href=\"https://doi.org/10.1523/JNEUROSCI.6104-11.2012\">https://doi.org/10.1523/JNEUROSCI.6104-11.2012</a>.","ieee":"S. Goswami, I. Bucurenciu, and P. M. Jonas, “Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling,” <i>Journal of Neuroscience</i>, vol. 32, no. 41. Society for Neuroscience, pp. 14294–14304, 2012.","short":"S. Goswami, I. Bucurenciu, P.M. Jonas, Journal of Neuroscience 32 (2012) 14294–14304.","mla":"Goswami, Sarit, et al. “Miniature IPSCs in Hippocampal Granule Cells Are Triggered by Voltage-Gated Ca^(2+) Channels via Microdomain Coupling.” <i>Journal of Neuroscience</i>, vol. 32, no. 41, Society for Neuroscience, 2012, pp. 14294–304, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.6104-11.2012\">10.1523/JNEUROSCI.6104-11.2012</a>.","ista":"Goswami S, Bucurenciu I, Jonas PM. 2012. Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling. Journal of Neuroscience. 32(41), 14294–14304."},"external_id":{"pmid":["23055500"]},"language":[{"iso":"eng"}],"oa_version":"Submitted Version","project":[{"name":"Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen","grant_number":"SFB-TR3-TP10B","_id":"25BDE9A4-B435-11E9-9278-68D0E5697425"}],"month":"10","publication":"Journal of Neuroscience","main_file_link":[{"open_access":"1","url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3632771/"}],"status":"public","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","publist_id":"3744","oa":1,"date_published":"2012-10-10T00:00:00Z","type":"journal_article"},{"publication":"Nature Neuroscience","oa_version":"Submitted Version","month":"09","language":[{"iso":"eng"}],"type":"journal_article","date_published":"2012-09-01T00:00:00Z","oa":1,"publist_id":"3578","main_file_link":[{"url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3431448/","open_access":"1"}],"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","status":"public","scopus_import":1,"_id":"3121","pmid":1,"issue":"9","author":[{"last_name":"Williams","first_name":"Courtney","full_name":"Williams, Courtney"},{"first_name":"Wenyan","last_name":"Chen","full_name":"Chen, Wenyan"},{"full_name":"Lee, Chia","first_name":"Chia","last_name":"Lee"},{"last_name":"Yaeger","first_name":"Daniel","full_name":"Yaeger, Daniel"},{"full_name":"Vyleta, Nicholas","last_name":"Vyleta","first_name":"Nicholas","id":"36C4978E-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Smith, Stephen","first_name":"Stephen","last_name":"Smith"}],"department":[{"_id":"PeJo"}],"date_created":"2018-12-11T12:01:30Z","publication_status":"published","intvolume":"        15","title":"Coactivation of multiple tightly coupled calcium channels triggers spontaneous release of GABA","quality_controlled":"1","page":"1195 - 1197","publisher":"Nature Publishing Group","year":"2012","citation":{"short":"C. Williams, W. Chen, C. Lee, D. Yaeger, N. Vyleta, S. Smith, Nature Neuroscience 15 (2012) 1195–1197.","mla":"Williams, Courtney, et al. “Coactivation of Multiple Tightly Coupled Calcium Channels Triggers Spontaneous Release of GABA.” <i>Nature Neuroscience</i>, vol. 15, no. 9, Nature Publishing Group, 2012, pp. 1195–97, doi:<a href=\"https://doi.org/10.1038/nn.3162\">10.1038/nn.3162</a>.","ista":"Williams C, Chen W, Lee C, Yaeger D, Vyleta N, Smith S. 2012. Coactivation of multiple tightly coupled calcium channels triggers spontaneous release of GABA. Nature Neuroscience. 15(9), 1195–1197.","apa":"Williams, C., Chen, W., Lee, C., Yaeger, D., Vyleta, N., &#38; Smith, S. (2012). Coactivation of multiple tightly coupled calcium channels triggers spontaneous release of GABA. <i>Nature Neuroscience</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/nn.3162\">https://doi.org/10.1038/nn.3162</a>","ama":"Williams C, Chen W, Lee C, Yaeger D, Vyleta N, Smith S. Coactivation of multiple tightly coupled calcium channels triggers spontaneous release of GABA. <i>Nature Neuroscience</i>. 2012;15(9):1195-1197. doi:<a href=\"https://doi.org/10.1038/nn.3162\">10.1038/nn.3162</a>","chicago":"Williams, Courtney, Wenyan Chen, Chia Lee, Daniel Yaeger, Nicholas Vyleta, and Stephen Smith. “Coactivation of Multiple Tightly Coupled Calcium Channels Triggers Spontaneous Release of GABA.” <i>Nature Neuroscience</i>. Nature Publishing Group, 2012. <a href=\"https://doi.org/10.1038/nn.3162\">https://doi.org/10.1038/nn.3162</a>.","ieee":"C. Williams, W. Chen, C. Lee, D. Yaeger, N. Vyleta, and S. Smith, “Coactivation of multiple tightly coupled calcium channels triggers spontaneous release of GABA,” <i>Nature Neuroscience</i>, vol. 15, no. 9. Nature Publishing Group, pp. 1195–1197, 2012."},"date_updated":"2021-01-12T07:41:12Z","external_id":{"pmid":["22842148"]},"day":"01","doi":"10.1038/nn.3162","abstract":[{"lang":"eng","text":"Voltage-activated Ca(2+) channels (VACCs) mediate Ca(2+) influx to trigger action potential-evoked neurotransmitter release, but the mechanism by which Ca(2+) regulates spontaneous transmission is unclear. We found that VACCs are the major physiological triggers for spontaneous release at mouse neocortical inhibitory synapses. Moreover, despite the absence of a synchronizing action potential, we found that spontaneous fusion of a GABA-containing vesicle required the activation of multiple tightly coupled VACCs of variable type."}],"volume":15,"acknowledgement":"The work was supported by the US National Institutes of Health (DA027110 and GM097433) and OCTRI. C.W. and N.P.V. were supported by a grant from the National Heart, Lung, and Blood Institute (T32HL033808).\r\nWe thank M. Andresen and K. Khodakhah for helpful comments. "},{"publication_identifier":{"issn":["1546-1726"]},"oa":1,"publist_id":"3390","date_published":"2012-04-01T00:00:00Z","type":"journal_article","main_file_link":[{"url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617474/","open_access":"1"}],"status":"public","related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"2964"}]},"user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","oa_version":"Published Version","project":[{"name":"Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen","grant_number":"SFB-TR3-TP10B","_id":"25BDE9A4-B435-11E9-9278-68D0E5697425"}],"month":"04","publication":"Nature Neuroscience","language":[{"iso":"eng"}],"doi":"10.1038/nn.3060","day":"01","abstract":[{"text":"CA3 pyramidal neurons are important for memory formation and pattern completion in the hippocampal network. It is generally thought that proximal synapses from the mossy fibers activate these neurons most efficiently, whereas distal inputs from the perforant path have a weaker modulatory influence. We used confocally targeted patch-clamp recording from dendrites and axons to map the activation of rat CA3 pyramidal neurons at the subcellular level. Our results reveal two distinct dendritic domains. In the proximal domain, action potentials initiated in the axon backpropagate actively with large amplitude and fast time course. In the distal domain, Na+ channel–mediated dendritic spikes are efficiently initiated by waveforms mimicking synaptic events. CA3 pyramidal neuron dendrites showed a high Na+-to-K+ conductance density ratio, providing ideal conditions for active backpropagation and dendritic spike initiation. Dendritic spikes may enhance the computational power of CA3 pyramidal neurons in the hippocampal network.","lang":"eng"}],"date_updated":"2023-09-07T11:43:52Z","year":"2012","citation":{"ista":"Kim S, Guzmán J, Hu H, Jonas PM. 2012. Active dendrites support efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons. Nature Neuroscience. 15(4), 600–606.","short":"S. Kim, J. Guzmán, H. Hu, P.M. Jonas, Nature Neuroscience 15 (2012) 600–606.","mla":"Kim, Sooyun, et al. “Active Dendrites Support Efficient Initiation of Dendritic Spikes in Hippocampal CA3 Pyramidal Neurons.” <i>Nature Neuroscience</i>, vol. 15, no. 4, Nature Publishing Group, 2012, pp. 600–06, doi:<a href=\"https://doi.org/10.1038/nn.3060\">10.1038/nn.3060</a>.","chicago":"Kim, Sooyun, José Guzmán, Hua Hu, and Peter M Jonas. “Active Dendrites Support Efficient Initiation of Dendritic Spikes in Hippocampal CA3 Pyramidal Neurons.” <i>Nature Neuroscience</i>. Nature Publishing Group, 2012. <a href=\"https://doi.org/10.1038/nn.3060\">https://doi.org/10.1038/nn.3060</a>.","ieee":"S. Kim, J. Guzmán, H. Hu, and P. M. Jonas, “Active dendrites support efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons,” <i>Nature Neuroscience</i>, vol. 15, no. 4. Nature Publishing Group, pp. 600–606, 2012.","ama":"Kim S, Guzmán J, Hu H, Jonas PM. Active dendrites support efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons. <i>Nature Neuroscience</i>. 2012;15(4):600-606. doi:<a href=\"https://doi.org/10.1038/nn.3060\">10.1038/nn.3060</a>","apa":"Kim, S., Guzmán, J., Hu, H., &#38; Jonas, P. M. (2012). Active dendrites support efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons. <i>Nature Neuroscience</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/nn.3060\">https://doi.org/10.1038/nn.3060</a>"},"external_id":{"pmid":["22388958"]},"acknowledgement":"This work was supported by the Deutsche Forschungsgemeinschaft (TR 3/B10) and the European Union (European Research Council Advanced grant to P.J.).","volume":15,"publication_status":"published","date_created":"2018-12-11T12:02:18Z","department":[{"_id":"PeJo"}],"article_processing_charge":"No","title":"Active dendrites support efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons","intvolume":"        15","_id":"3258","pmid":1,"scopus_import":"1","author":[{"id":"394AB1C8-F248-11E8-B48F-1D18A9856A87","full_name":"Kim, Sooyun","first_name":"Sooyun","last_name":"Kim"},{"last_name":"Guzmán","first_name":"José","full_name":"Guzmán, José","orcid":"0000-0003-2209-5242","id":"30CC5506-F248-11E8-B48F-1D18A9856A87"},{"id":"4AC0145C-F248-11E8-B48F-1D18A9856A87","first_name":"Hua","last_name":"Hu","full_name":"Hu, Hua"},{"full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804","last_name":"Jonas","first_name":"Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"}],"issue":"4","publisher":"Nature Publishing Group","article_type":"original","page":"600 - 606","quality_controlled":"1"},{"date_updated":"2021-01-12T07:42:36Z","year":"2012","citation":{"mla":"Eggermann, Emmanuel, et al. “Nanodomain Coupling between Ca(2+) Channels and Sensors of Exocytosis at Fast Mammalian Synapses.” <i>Nature Reviews Neuroscience</i>, vol. 13, no. 1, Nature Publishing Group, 2012, pp. 7–21, doi:<a href=\"https://doi.org/10.1038/nrn3125\">10.1038/nrn3125</a>.","short":"E. Eggermann, I. Bucurenciu, S. Goswami, P.M. Jonas, Nature Reviews Neuroscience 13 (2012) 7–21.","ista":"Eggermann E, Bucurenciu I, Goswami S, Jonas PM. 2012. Nanodomain coupling between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses. Nature Reviews Neuroscience. 13(1), 7–21.","ama":"Eggermann E, Bucurenciu I, Goswami S, Jonas PM. Nanodomain coupling between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses. <i>Nature Reviews Neuroscience</i>. 2012;13(1):7-21. doi:<a href=\"https://doi.org/10.1038/nrn3125\">10.1038/nrn3125</a>","apa":"Eggermann, E., Bucurenciu, I., Goswami, S., &#38; Jonas, P. M. (2012). Nanodomain coupling between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses. <i>Nature Reviews Neuroscience</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/nrn3125\">https://doi.org/10.1038/nrn3125</a>","ieee":"E. Eggermann, I. Bucurenciu, S. Goswami, and P. M. Jonas, “Nanodomain coupling between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses,” <i>Nature Reviews Neuroscience</i>, vol. 13, no. 1. Nature Publishing Group, pp. 7–21, 2012.","chicago":"Eggermann, Emmanuel, Iancu Bucurenciu, Sarit Goswami, and Peter M Jonas. “Nanodomain Coupling between Ca(2+) Channels and Sensors of Exocytosis at Fast Mammalian Synapses.” <i>Nature Reviews Neuroscience</i>. Nature Publishing Group, 2012. <a href=\"https://doi.org/10.1038/nrn3125\">https://doi.org/10.1038/nrn3125</a>."},"abstract":[{"lang":"eng","text":"The physical distance between presynaptic Ca2+ channels and the Ca2+ sensors that trigger exocytosis of neurotransmitter-containing vesicles is a key determinant of the signalling properties of synapses in the nervous system. Recent functional analysis indicates that in some fast central synapses, transmitter release is triggered by a small number of Ca2+ channels that are coupled to Ca2+ sensors at the nanometre scale. Molecular analysis suggests that this tight coupling is generated by protein–protein interactions involving Ca2+ channels, Ca2+ sensors and various other synaptic proteins. Nanodomain coupling has several functional advantages, as it increases the efficacy, speed and energy efficiency of synaptic transmission."}],"doi":"10.1038/nrn3125","day":"01","ddc":["570"],"acknowledgement":"Work of the authors was funded by grants of the Deutsche Forschungsgemeinschaft to P.J. (grants SFB 780/A5, TR 3/B10 and the Leibniz programme), a European Research Council Advanced grant to P.J. and a Swiss National Foundation fellowship to E.E.\r\nWe thank D. Tsien and E. Neher for their comments on this Review, J. Guzmán and A. Pernía-Andrade for reading earlier versions and E. Kramberger for perfect editorial support. We apologize that owing to space constraints, not all relevant papers could be cited.\r\n","volume":13,"author":[{"id":"34DACA34-E9AE-11E9-849C-D35BD8ADC20C","last_name":"Eggermann","first_name":"Emmanuel","full_name":"Eggermann, Emmanuel"},{"id":"4BD1D872-E9AE-11E9-9EE9-8BF4597A9E2A","full_name":"Bucurenciu, Iancu","first_name":"Iancu","last_name":"Bucurenciu"},{"last_name":"Goswami","first_name":"Sarit","full_name":"Goswami, Sarit","id":"3A578F32-F248-11E8-B48F-1D18A9856A87"},{"id":"353C1B58-F248-11E8-B48F-1D18A9856A87","first_name":"Peter M","last_name":"Jonas","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M"}],"issue":"1","_id":"3317","scopus_import":1,"title":"Nanodomain coupling between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses","pubrep_id":"820","intvolume":"        13","publication_status":"published","department":[{"_id":"PeJo"}],"date_created":"2018-12-11T12:02:38Z","file_date_updated":"2020-07-14T12:46:07Z","page":"7 - 21","quality_controlled":"1","publisher":"Nature Publishing Group","date_published":"2012-01-01T00:00:00Z","type":"journal_article","oa":1,"publist_id":"3322","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","status":"public","file":[{"content_type":"application/pdf","file_name":"IST-2017-820-v1+1_17463_3_art_file_109404_ltmxbw.pdf","date_updated":"2020-07-14T12:46:07Z","checksum":"4c1c86b2f6e4e1562f5bb800b457ea9f","file_size":314246,"date_created":"2018-12-12T10:12:13Z","creator":"system","file_id":"4931","relation":"main_file","access_level":"open_access"},{"date_updated":"2020-07-14T12:46:07Z","content_type":"application/pdf","file_name":"IST-2017-820-v1+2_17463_3_figure_109402_ltmwlp.pdf","date_created":"2018-12-12T10:12:14Z","file_size":1840216,"checksum":"bceb2efdd49d115f4dde8486bc1be3f2","file_id":"4932","creator":"system","relation":"main_file","access_level":"open_access"}],"publication":"Nature Reviews Neuroscience","has_accepted_license":"1","month":"01","oa_version":"Submitted Version","project":[{"name":"Synaptic Mechanisms of Neuronal Network Function","grant_number":"JO_780/A5","_id":"25BC64A8-B435-11E9-9278-68D0E5697425"},{"_id":"25BDE9A4-B435-11E9-9278-68D0E5697425","name":"Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen","grant_number":"SFB-TR3-TP10B"}],"language":[{"iso":"eng"}]},{"intvolume":"         6","title":"Review of the BCI competition IV","pubrep_id":"945","date_created":"2018-12-11T11:46:46Z","department":[{"_id":"ScienComp"},{"_id":"PeJo"}],"publication_status":"published","author":[{"full_name":"Tangermann, Michael","last_name":"Tangermann","first_name":"Michael"},{"full_name":"Müller, Klaus","first_name":"Klaus","last_name":"Müller"},{"first_name":"Ad","last_name":"Aertsen","full_name":"Aertsen, Ad"},{"last_name":"Birbaumer","first_name":"Niels","full_name":"Birbaumer, Niels"},{"full_name":"Braun, Christoph","first_name":"Christoph","last_name":"Braun"},{"full_name":"Brunner, Clemens","first_name":"Clemens","last_name":"Brunner"},{"last_name":"Leeb","first_name":"Robert","full_name":"Leeb, Robert"},{"full_name":"Mehring, Carsten","first_name":"Carsten","last_name":"Mehring"},{"first_name":"Kai","last_name":"Miller","full_name":"Miller, Kai"},{"full_name":"Müller Putz, Gernot","first_name":"Gernot","last_name":"Müller Putz"},{"last_name":"Nolte","first_name":"Guido","full_name":"Nolte, Guido"},{"first_name":"Gert","last_name":"Pfurtscheller","full_name":"Pfurtscheller, Gert"},{"full_name":"Preissl, Hubert","first_name":"Hubert","last_name":"Preissl"},{"full_name":"Schalk, Gerwin","first_name":"Gerwin","last_name":"Schalk"},{"last_name":"Schlögl","first_name":"Alois","full_name":"Schlögl, Alois","orcid":"0000-0002-5621-8100","id":"45BF87EE-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Vidaurre","first_name":"Carmen","full_name":"Vidaurre, Carmen"},{"full_name":"Waldert, Stephan","first_name":"Stephan","last_name":"Waldert"},{"first_name":"Benjamin","last_name":"Blankertz","full_name":"Blankertz, Benjamin"}],"scopus_import":1,"_id":"493","publisher":"Frontiers Research Foundation","file_date_updated":"2020-07-14T12:46:35Z","quality_controlled":"1","abstract":[{"text":"The BCI competition IV stands in the tradition of prior BCI competitions that aim to provide high quality neuroscientific data for open access to the scientific community. As experienced already in prior competitions not only scientists from the narrow field of BCI compete, but scholars with a broad variety of backgrounds and nationalities. They include high specialists as well as students.The goals of all BCI competitions have always been to challenge with respect to novel paradigms and complex data. We report on the following challenges: (1) asynchronous data, (2) synthetic, (3) multi-class continuous data, (4) sessionto-session transfer, (5) directionally modulated MEG, (6) finger movements recorded by ECoG. As after past competitions, our hope is that winning entries may enhance the analysis methods of future BCIs.","lang":"eng"}],"day":"13","doi":"10.3389/fnins.2012.00055","citation":{"ista":"Tangermann M, Müller K, Aertsen A, Birbaumer N, Braun C, Brunner C, Leeb R, Mehring C, Miller K, Müller Putz G, Nolte G, Pfurtscheller G, Preissl H, Schalk G, Schlögl A, Vidaurre C, Waldert S, Blankertz B. 2012. Review of the BCI competition IV. Frontiers in Neuroscience. 6, 55.","mla":"Tangermann, Michael, et al. “Review of the BCI Competition IV.” <i>Frontiers in Neuroscience</i>, vol. 6, 55, Frontiers Research Foundation, 2012, doi:<a href=\"https://doi.org/10.3389/fnins.2012.00055\">10.3389/fnins.2012.00055</a>.","short":"M. Tangermann, K. Müller, A. Aertsen, N. Birbaumer, C. Braun, C. Brunner, R. Leeb, C. Mehring, K. Miller, G. Müller Putz, G. Nolte, G. Pfurtscheller, H. Preissl, G. Schalk, A. Schlögl, C. Vidaurre, S. Waldert, B. Blankertz, Frontiers in Neuroscience 6 (2012).","chicago":"Tangermann, Michael, Klaus Müller, Ad Aertsen, Niels Birbaumer, Christoph Braun, Clemens Brunner, Robert Leeb, et al. “Review of the BCI Competition IV.” <i>Frontiers in Neuroscience</i>. Frontiers Research Foundation, 2012. <a href=\"https://doi.org/10.3389/fnins.2012.00055\">https://doi.org/10.3389/fnins.2012.00055</a>.","ieee":"M. Tangermann <i>et al.</i>, “Review of the BCI competition IV,” <i>Frontiers in Neuroscience</i>, vol. 6. Frontiers Research Foundation, 2012.","apa":"Tangermann, M., Müller, K., Aertsen, A., Birbaumer, N., Braun, C., Brunner, C., … Blankertz, B. (2012). Review of the BCI competition IV. <i>Frontiers in Neuroscience</i>. Frontiers Research Foundation. <a href=\"https://doi.org/10.3389/fnins.2012.00055\">https://doi.org/10.3389/fnins.2012.00055</a>","ama":"Tangermann M, Müller K, Aertsen A, et al. Review of the BCI competition IV. <i>Frontiers in Neuroscience</i>. 2012;6. doi:<a href=\"https://doi.org/10.3389/fnins.2012.00055\">10.3389/fnins.2012.00055</a>"},"year":"2012","date_updated":"2021-01-12T08:01:03Z","ddc":["004"],"volume":6,"acknowledgement":"The studies were in part or completely supported by the Bundesministerium für Bildung und Forschung (BMBF), Fkz 01IB001A, 01GQ0850, by the German Science Foundation (DFG, contract MU 987/3-2), by the European ICT Programme Projects FP7-224631 and 216886, the World Class University Program through the National Research Foundation of Korea funded by the Ministry of Education, Science, and Technology (Grant R31-10008), the US Army Research Office [W911NF-08-1-0216 (Gerwin Schalk) and W911NF-07-1-0415 (Gerwin Schalk)] and the NIH [EB006356 (Gerwin Schalk) and EB000856 (Gerwin Schalk), the WIN-Kolleg of the Heidelberg Academy of Sciences and Humanities, German Federal Ministry of Education and Research grants 01GQ0420, 01GQ0761, 01GQ0762, and 01GQ0830, German Research Foundation grants 550/B5 and C6, and by a scholarship from the German National Academic Foundation. This paper only reflects the authors’ views and funding agencies are not liable for any use that may be made of the information contained herein.\r\n","article_number":"55","month":"07","oa_version":"Published Version","has_accepted_license":"1","publication":"Frontiers in Neuroscience","language":[{"iso":"eng"}],"oa":1,"publist_id":"7327","type":"journal_article","date_published":"2012-07-13T00:00:00Z","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"status":"public","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","file":[{"access_level":"open_access","relation":"main_file","file_id":"5356","creator":"system","date_created":"2018-12-12T10:18:34Z","checksum":"195238221c4b0b0f4035f6f6c16ea17c","file_size":2693701,"date_updated":"2020-07-14T12:46:35Z","file_name":"IST-2018-945-v1+1_2012_Schloegl_Review_of.pdf","content_type":"application/pdf"}]},{"publication":"Nature Neuroscience","_id":"3318","scopus_import":1,"author":[{"full_name":"Eggermann, Emmanuel","last_name":"Eggermann","first_name":"Emmanuel"},{"id":"353C1B58-F248-11E8-B48F-1D18A9856A87","full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804","last_name":"Jonas","first_name":"Peter M"}],"publication_status":"published","oa_version":"Submitted Version","date_created":"2018-12-11T12:02:38Z","department":[{"_id":"PeJo"}],"title":"How the “slow” Ca(2+) buffer parvalbumin affects transmitter release in nanodomain coupling regimes at GABAergic synapses","month":"12","intvolume":"        15","page":"20 - 22","quality_controlled":"1","language":[{"iso":"eng"}],"publisher":"Nature Publishing Group","date_updated":"2021-01-12T07:42:37Z","citation":{"apa":"Eggermann, E., &#38; Jonas, P. M. (2011). How the “slow” Ca(2+) buffer parvalbumin affects transmitter release in nanodomain coupling regimes at GABAergic synapses. <i>Nature Neuroscience</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/nn.3002\">https://doi.org/10.1038/nn.3002</a>","ama":"Eggermann E, Jonas PM. How the “slow” Ca(2+) buffer parvalbumin affects transmitter release in nanodomain coupling regimes at GABAergic synapses. <i>Nature Neuroscience</i>. 2011;15:20-22. doi:<a href=\"https://doi.org/10.1038/nn.3002\">10.1038/nn.3002</a>","chicago":"Eggermann, Emmanuel, and Peter M Jonas. “How the ‘Slow’ Ca(2+) Buffer Parvalbumin Affects Transmitter Release in Nanodomain Coupling Regimes at GABAergic Synapses.” <i>Nature Neuroscience</i>. Nature Publishing Group, 2011. <a href=\"https://doi.org/10.1038/nn.3002\">https://doi.org/10.1038/nn.3002</a>.","ieee":"E. Eggermann and P. M. Jonas, “How the ‘slow’ Ca(2+) buffer parvalbumin affects transmitter release in nanodomain coupling regimes at GABAergic synapses,” <i>Nature Neuroscience</i>, vol. 15. Nature Publishing Group, pp. 20–22, 2011.","short":"E. Eggermann, P.M. Jonas, Nature Neuroscience 15 (2011) 20–22.","mla":"Eggermann, Emmanuel, and Peter M. Jonas. “How the ‘Slow’ Ca(2+) Buffer Parvalbumin Affects Transmitter Release in Nanodomain Coupling Regimes at GABAergic Synapses.” <i>Nature Neuroscience</i>, vol. 15, Nature Publishing Group, 2011, pp. 20–22, doi:<a href=\"https://doi.org/10.1038/nn.3002\">10.1038/nn.3002</a>.","ista":"Eggermann E, Jonas PM. 2011. How the “slow” Ca(2+) buffer parvalbumin affects transmitter release in nanodomain coupling regimes at GABAergic synapses. Nature Neuroscience. 15, 20–22."},"year":"2011","date_published":"2011-12-04T00:00:00Z","type":"journal_article","doi":"10.1038/nn.3002","day":"04","abstract":[{"text":"Parvalbumin is thought to act in a manner similar to EGTA, but how a slow Ca2+ buffer affects nanodomain-coupling regimes at GABAergic synapses is unclear. Direct measurements of parvalbumin concentration and paired recordings in rodent hippocampus and cerebellum revealed that parvalbumin affects synaptic dynamics only when expressed at high levels. Modeling suggests that, in high concentrations, parvalbumin may exert BAPTA-like effects, modulating nanodomain coupling via competition with local saturation of endogenous fixed buffers.","lang":"eng"}],"oa":1,"publist_id":"3321","volume":15,"main_file_link":[{"open_access":"1","url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3631701/"}],"status":"public","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87"},{"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","status":"public","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3097128/","open_access":"1"}],"volume":31,"type":"journal_article","date_published":"2011-03-23T00:00:00Z","year":"2011","citation":{"chicago":"Vyleta, Nicholas, and Stephen Smith. “Spontaneous Glutamate Release Is Independent of Calcium Influx and Tonically Activated by the Calcium-Sensing Receptor.” <i>European Journal of Neuroscience</i>. Wiley-Blackwell, 2011. <a href=\"https://doi.org/10.1523/JNEUROSCI.6398-10.2011\">https://doi.org/10.1523/JNEUROSCI.6398-10.2011</a>.","ieee":"N. Vyleta and S. Smith, “Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor,” <i>European Journal of Neuroscience</i>, vol. 31, no. 12. Wiley-Blackwell, pp. 4593–4606, 2011.","ama":"Vyleta N, Smith S. Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor. <i>European Journal of Neuroscience</i>. 2011;31(12):4593-4606. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.6398-10.2011\">10.1523/JNEUROSCI.6398-10.2011</a>","apa":"Vyleta, N., &#38; Smith, S. (2011). Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor. <i>European Journal of Neuroscience</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1523/JNEUROSCI.6398-10.2011\">https://doi.org/10.1523/JNEUROSCI.6398-10.2011</a>","ista":"Vyleta N, Smith S. 2011. Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor. European Journal of Neuroscience. 31(12), 4593–4606.","mla":"Vyleta, Nicholas, and Stephen Smith. “Spontaneous Glutamate Release Is Independent of Calcium Influx and Tonically Activated by the Calcium-Sensing Receptor.” <i>European Journal of Neuroscience</i>, vol. 31, no. 12, Wiley-Blackwell, 2011, pp. 4593–606, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.6398-10.2011\">10.1523/JNEUROSCI.6398-10.2011</a>.","short":"N. Vyleta, S. Smith, European Journal of Neuroscience 31 (2011) 4593–4606."},"date_updated":"2021-01-12T08:00:49Z","publist_id":"7353","oa":1,"abstract":[{"lang":"eng","text":"Spontaneous release of glutamate is important for maintaining synaptic strength and controlling spike timing in the brain. Mechanisms regulating spontaneous exocytosis remain poorly understood. Extracellular calcium concentration ([Ca2+]o) regulates Ca2+ entry through voltage-activated calcium channels (VACCs) and consequently is a pivotal determinant of action potential-evoked vesicle fusion. Extracellular Ca 2+ also enhances spontaneous release, but via unknown mechanisms. Here we report that external Ca2+ triggers spontaneous glutamate release more weakly than evoked release in mouse neocortical neurons. Blockade of VACCs has no effect on the spontaneous release rate or its dependence on [Ca2+]o. Intracellular [Ca2+] slowly increases in a minority of neurons following increases in [Ca2+]o. Furthermore, the enhancement of spontaneous release by extracellular calcium is insensitive to chelation of intracellular calcium by BAPTA. Activation of the calcium-sensing receptor (CaSR), a G-protein-coupled receptor present in nerve terminals, by several specific agonists increased spontaneous glutamate release. The frequency of spontaneous synaptic transmission was decreased in CaSR mutant neurons. The concentration-effect relationship for extracellular calcium regulation of spontaneous release was well described by a combination of CaSR-dependent and CaSR-independent mechanisms. Overall these results indicate that extracellular Ca2+ does not trigger spontaneous glutamate release by simply increasing calcium influx but stimulates CaSR and thereby promotes resting spontaneous glutamate release. "}],"day":"23","doi":"10.1523/JNEUROSCI.6398-10.2011","language":[{"iso":"eng"}],"quality_controlled":"1","page":"4593 - 4606","publisher":"Wiley-Blackwell","issue":"12","author":[{"id":"36C4978E-F248-11E8-B48F-1D18A9856A87","full_name":"Vyleta, Nicholas","last_name":"Vyleta","first_name":"Nicholas"},{"last_name":"Smith","first_name":"Stephen","full_name":"Smith, Stephen"}],"scopus_import":1,"_id":"469","publication":"European Journal of Neuroscience","intvolume":"        31","title":"Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor","month":"03","department":[{"_id":"PeJo"}],"date_created":"2018-12-11T11:46:39Z","publication_status":"published","oa_version":"Submitted Version"},{"volume":2011,"ddc":["005"],"day":"01","doi":"10.1155/2011/935364","abstract":[{"text":"BioSig is an open source software library for biomedical signal processing. The aim of the BioSig project is to foster research in biomedical signal processing by providing free and open source software tools for many different application areas. Some of the areas where BioSig can be employed are neuroinformatics, brain-computer interfaces, neurophysiology, psychology, cardiovascular systems, and sleep research. Moreover, the analysis of biosignals such as the electroencephalogram (EEG), electrocorticogram (ECoG), electrocardiogram (ECG), electrooculogram (EOG), electromyogram (EMG), or respiration signals is a very relevant element of the BioSig project. Specifically, BioSig provides solutions for data acquisition, artifact processing, quality control, feature extraction, classification, modeling, and data visualization, to name a few. In this paper, we highlight several methods to help students and researchers to work more efficiently with biomedical signals. ","lang":"eng"}],"citation":{"mla":"Schlögl, Alois, et al. “BioSig: The Free and Open Source Software Library for Biomedical Signal Processing.” <i>Computational Intelligence and Neuroscience</i>, vol. 2011, 935364, Hindawi Publishing Corporation, 2011, doi:<a href=\"https://doi.org/10.1155/2011/935364\">10.1155/2011/935364</a>.","short":"A. Schlögl, C. Vidaurre, T. Sander, Computational Intelligence and Neuroscience 2011 (2011).","ista":"Schlögl A, Vidaurre C, Sander T. 2011. BioSig: The free and open source software library for biomedical signal processing. Computational Intelligence and Neuroscience. 2011, 935364.","ama":"Schlögl A, Vidaurre C, Sander T. BioSig: The free and open source software library for biomedical signal processing. <i>Computational Intelligence and Neuroscience</i>. 2011;2011. doi:<a href=\"https://doi.org/10.1155/2011/935364\">10.1155/2011/935364</a>","apa":"Schlögl, A., Vidaurre, C., &#38; Sander, T. (2011). BioSig: The free and open source software library for biomedical signal processing. <i>Computational Intelligence and Neuroscience</i>. Hindawi Publishing Corporation. <a href=\"https://doi.org/10.1155/2011/935364\">https://doi.org/10.1155/2011/935364</a>","ieee":"A. Schlögl, C. Vidaurre, and T. Sander, “BioSig: The free and open source software library for biomedical signal processing,” <i>Computational Intelligence and Neuroscience</i>, vol. 2011. Hindawi Publishing Corporation, 2011.","chicago":"Schlögl, Alois, Carmen Vidaurre, and Tilmann Sander. “BioSig: The Free and Open Source Software Library for Biomedical Signal Processing.” <i>Computational Intelligence and Neuroscience</i>. Hindawi Publishing Corporation, 2011. <a href=\"https://doi.org/10.1155/2011/935364\">https://doi.org/10.1155/2011/935364</a>."},"year":"2011","date_updated":"2021-01-12T08:01:02Z","publisher":"Hindawi Publishing Corporation","quality_controlled":"1","file_date_updated":"2020-07-14T12:46:35Z","date_created":"2018-12-11T11:46:45Z","department":[{"_id":"ScienComp"},{"_id":"PeJo"}],"publication_status":"published","intvolume":"      2011","title":"BioSig: The free and open source software library for biomedical signal processing","pubrep_id":"947","scopus_import":1,"_id":"490","author":[{"full_name":"Schlögl, Alois","orcid":"0000-0002-5621-8100","last_name":"Schlögl","first_name":"Alois","id":"45BF87EE-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Vidaurre, Carmen","first_name":"Carmen","last_name":"Vidaurre"},{"full_name":"Sander, Tilmann","first_name":"Tilmann","last_name":"Sander"}],"file":[{"file_id":"4642","creator":"system","relation":"main_file","access_level":"open_access","date_updated":"2020-07-14T12:46:35Z","file_name":"IST-2018-947-v1+1_2011_Schloegl_BioSig.pdf","content_type":"application/pdf","date_created":"2018-12-12T10:07:44Z","file_size":2863551,"checksum":"8263bbf255171f2054f43f3db5f53b6e"}],"status":"public","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","oa":1,"publist_id":"7330","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"type":"journal_article","date_published":"2011-01-01T00:00:00Z","language":[{"iso":"eng"}],"oa_version":"Published Version","article_number":"935364","month":"01","has_accepted_license":"1","publication":"Computational Intelligence and Neuroscience"},{"volume":69,"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","status":"public","doi":"10.1016/j.neuron.2011.01.010","day":"27","abstract":[{"text":"Rab3 interacting molecules (RIMs) are highly enriched in the active zones of presynaptic terminals. It is generally thought that they operate as effectors of the small G protein Rab3. Three recent papers, by Han et al. (this issue of Neuron), Deng et al. (this issue of Neuron), and Kaeser et al. (a recent issue of Cell), shed new light on the functional role of RIM in presynaptic terminals. First, RIM tethers Ca2+ channels to active zones. Second, RIM contributes to priming of synaptic vesicles by interacting with another presynaptic protein, Munc13.","lang":"eng"}],"publist_id":"3243","date_updated":"2021-01-12T07:43:00Z","citation":{"short":"A. Pernia-Andrade, P.M. Jonas, Neuron 69 (2011) 185–187.","mla":"Pernia-Andrade, Alejandro, and Peter M. Jonas. “The Multiple Faces of RIM.” <i>Neuron</i>, vol. 69, no. 2, Elsevier, 2011, pp. 185–87, doi:<a href=\"https://doi.org/10.1016/j.neuron.2011.01.010\">10.1016/j.neuron.2011.01.010</a>.","ista":"Pernia-Andrade A, Jonas PM. 2011. The multiple faces of RIM. Neuron. 69(2), 185–187.","apa":"Pernia-Andrade, A., &#38; Jonas, P. M. (2011). The multiple faces of RIM. <i>Neuron</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuron.2011.01.010\">https://doi.org/10.1016/j.neuron.2011.01.010</a>","ama":"Pernia-Andrade A, Jonas PM. The multiple faces of RIM. <i>Neuron</i>. 2011;69(2):185-187. doi:<a href=\"https://doi.org/10.1016/j.neuron.2011.01.010\">10.1016/j.neuron.2011.01.010</a>","ieee":"A. Pernia-Andrade and P. M. Jonas, “The multiple faces of RIM,” <i>Neuron</i>, vol. 69, no. 2. Elsevier, pp. 185–187, 2011.","chicago":"Pernia-Andrade, Alejandro, and Peter M Jonas. “The Multiple Faces of RIM.” <i>Neuron</i>. Elsevier, 2011. <a href=\"https://doi.org/10.1016/j.neuron.2011.01.010\">https://doi.org/10.1016/j.neuron.2011.01.010</a>."},"year":"2011","date_published":"2011-01-27T00:00:00Z","type":"journal_article","publisher":"Elsevier","page":"185 - 187","quality_controlled":"1","language":[{"iso":"eng"}],"publication_status":"published","oa_version":"None","date_created":"2018-12-11T12:02:56Z","department":[{"_id":"PeJo"}],"month":"01","title":"The multiple faces of RIM","intvolume":"        69","_id":"3369","publication":"Neuron","scopus_import":1,"author":[{"id":"36963E98-F248-11E8-B48F-1D18A9856A87","full_name":"Pernia-Andrade, Alejandro","first_name":"Alejandro","last_name":"Pernia-Andrade"},{"id":"353C1B58-F248-11E8-B48F-1D18A9856A87","first_name":"Peter M","last_name":"Jonas","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M"}],"issue":"2"},{"abstract":[{"lang":"eng","text":"Long-term depression (LTD) is a form of synaptic plasticity that may contribute to information storage in the central nervous system. Here we report that LTD can be elicited in layer 5 pyramidal neurons of the rat prefrontal cortex by pairing low frequency stimulation with a modest postsynaptic depolarization. The induction of LTD required the activation of both metabotropic glutamate receptors of the mGlu1 subtype and voltage-sensitive Ca(2+) channels (VSCCs) of the T/R, P/Q and N types, leading to the stimulation of intracellular inositol trisphosphate (IP3) receptors by IP3 and Ca(2+). The subsequent release of Ca(2+) from intracellular stores activated the protein phosphatase cascade involving calcineurin and protein phosphatase 1. The activation of purinergic P2Y(1) receptors blocked LTD. This effect was prevented by P2Y(1) receptor antagonists and was absent in mice lacking P2Y(1) but not P2Y(2) receptors. We also found that activation of P2Y(1) receptors inhibits Ca(2+) transients via VSCCs in the apical dendrites and spines of pyramidal neurons. In addition, we show that the release of ATP under hypoxia is able to inhibit LTD by acting on postsynaptic P2Y(1) receptors. In conclusion, these data suggest that the reduction of Ca(2+) influx via VSCCs caused by the activation of P2Y(1) receptors by ATP is the possible mechanism for the inhibition of LTD in prefrontal cortex."}],"publist_id":"2512","doi":"10.1016/j.neuropharm.2010.05.013","day":"01","date_published":"2010-11-01T00:00:00Z","type":"journal_article","date_updated":"2021-01-12T07:51:42Z","citation":{"ieee":"J. Guzmán <i>et al.</i>, “P2Y1 receptors inhibit long-term depression in the prefrontal cortex.,” <i>Neuropharmacology</i>, vol. 59, no. 6. Elsevier, pp. 406–415, 2010.","chicago":"Guzmán, José, Hartmut Schmidt, Heike Franke, Ute Krügel, Jens Eilers, Peter Illes, and Zoltan Gerevich. “P2Y1 Receptors Inhibit Long-Term Depression in the Prefrontal Cortex.” <i>Neuropharmacology</i>. Elsevier, 2010. <a href=\"https://doi.org/10.1016/j.neuropharm.2010.05.013\">https://doi.org/10.1016/j.neuropharm.2010.05.013</a>.","apa":"Guzmán, J., Schmidt, H., Franke, H., Krügel, U., Eilers, J., Illes, P., &#38; Gerevich, Z. (2010). P2Y1 receptors inhibit long-term depression in the prefrontal cortex. <i>Neuropharmacology</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuropharm.2010.05.013\">https://doi.org/10.1016/j.neuropharm.2010.05.013</a>","ama":"Guzmán J, Schmidt H, Franke H, et al. P2Y1 receptors inhibit long-term depression in the prefrontal cortex. <i>Neuropharmacology</i>. 2010;59(6):406-415. doi:<a href=\"https://doi.org/10.1016/j.neuropharm.2010.05.013\">10.1016/j.neuropharm.2010.05.013</a>","ista":"Guzmán J, Schmidt H, Franke H, Krügel U, Eilers J, Illes P, Gerevich Z. 2010. P2Y1 receptors inhibit long-term depression in the prefrontal cortex. Neuropharmacology. 59(6), 406–415.","short":"J. Guzmán, H. Schmidt, H. Franke, U. Krügel, J. Eilers, P. Illes, Z. Gerevich, Neuropharmacology 59 (2010) 406–415.","mla":"Guzmán, José, et al. “P2Y1 Receptors Inhibit Long-Term Depression in the Prefrontal Cortex.” <i>Neuropharmacology</i>, vol. 59, no. 6, Elsevier, 2010, pp. 406–15, doi:<a href=\"https://doi.org/10.1016/j.neuropharm.2010.05.013\">10.1016/j.neuropharm.2010.05.013</a>."},"year":"2010","status":"public","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","volume":59,"acknowledgement":" The financial support of the Deutsche Forschungsgemeinschaft (IL 20/12-1, KI 677/2-4) is gratefully acknowledged.\r\nWe thank B. H. Koller (Department of Genetics and Molecular Biology, University of North Carolina at Chapel Hill, NC, USA) for the generous supply of P2Y1−/− and P2Y2−/− mice. We are grateful to Dr. A. Schulz for reanalysing the genotype of the P2Y1−/− mice. The authors thank P. Jonas and U. Heinemann for many helpful comments and A-K. Krause, L Feige and M. Eberts for their excellent technical support.","month":"11","title":"P2Y1 receptors inhibit long-term depression in the prefrontal cortex.","intvolume":"        59","oa_version":"None","publication_status":"published","department":[{"_id":"PeJo"}],"date_created":"2018-12-11T12:04:47Z","author":[{"id":"30CC5506-F248-11E8-B48F-1D18A9856A87","first_name":"José","last_name":"Guzmán","full_name":"Guzmán, José"},{"last_name":"Schmidt","first_name":"Hartmut","full_name":"Schmidt, Hartmut"},{"full_name":"Franke, Heike","last_name":"Franke","first_name":"Heike"},{"last_name":"Krügel","first_name":"Ute","full_name":"Krügel, Ute"},{"last_name":"Eilers","first_name":"Jens","full_name":"Eilers, Jens"},{"last_name":"Illes","first_name":"Peter","full_name":"Illes, Peter"},{"last_name":"Gerevich","first_name":"Zoltan","full_name":"Gerevich, Zoltan"}],"issue":"6","_id":"3718","publication":"Neuropharmacology","scopus_import":1,"publisher":"Elsevier","language":[{"iso":"eng"}],"page":"406 - 415","quality_controlled":"1"}]