{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cho IH"],"funding":["HHS | NIH | National Institute of General Medical Sciences","HHS | NIH | National Institute of Neurological Disorders and Stroke","NINDS NIH HHS","NSF | BIO | Division of Integrative Organismal Systems","NIGMS NIH HHS","Esther A. and Joseph Klingenstein Fund","U.S. Department of Education"],"pagination":["29937-29947"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7703594"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["117(47)"],"pubmed_abstract":["Analysis of the presynaptic action potential's (AP<sub>syn</sub>) role in synaptic facilitation in hippocampal pyramidal neurons has been difficult due to size limitations of axons. We overcame these size barriers by combining high-resolution optical recordings of membrane potential, exocytosis, and Ca<sup>2+</sup> in cultured hippocampal neurons. These recordings revealed a critical and selective role for K<sub>v</sub>1 channel inactivation in synaptic facilitation of excitatory hippocampal neurons. Presynaptic K<sub>v</sub>1 channel inactivation was mediated by the K<sub>v</sub>β1 subunit and had a surprisingly rapid onset that was readily apparent even in brief physiological stimulation paradigms including paired-pulse stimulation. Genetic depletion of K<sub>v</sub>β1 blocked all broadening of the AP<sub>syn</sub> during high-frequency stimulation and eliminated synaptic facilitation without altering the initial probability of vesicle release. Thus, using all quantitative optical measurements of presynaptic physiology, we reveal a critical role for presynaptic K<sub>v</sub> channels in synaptic facilitation at presynaptic terminals of the hippocampus upstream of the exocytic machinery."],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["The potassium channel subunit K<sub>v</sub>β1 serves as a major control point for synaptic facilitation."],"pmcid":["PMC7703594"],"funding_grant_id":["F31NS110192-01A1","003","P20‐GM113132","R00‐NS099469","P200A150059","P20 GM113132","R00 NS099469","1750199","F31 NS110192"],"pubmed_authors":["Cho IH","Olveda GE","Hoppa MB","Panzera LC","Alpizar SA","Chin M","Hill RA"],"additional_accession":[]},"is_claimable":false,"name":"The potassium channel subunit K<sub>v</sub>β1 serves as a major control point for synaptic facilitation.","description":"Analysis of the presynaptic action potential's (AP<sub>syn</sub>) role in synaptic facilitation in hippocampal pyramidal neurons has been difficult due to size limitations of axons. We overcame these size barriers by combining high-resolution optical recordings of membrane potential, exocytosis, and Ca<sup>2+</sup> in cultured hippocampal neurons. These recordings revealed a critical and selective role for K<sub>v</sub>1 channel inactivation in synaptic facilitation of excitatory hippocampal neurons. Presynaptic K<sub>v</sub>1 channel inactivation was mediated by the K<sub>v</sub>β1 subunit and had a surprisingly rapid onset that was readily apparent even in brief physiological stimulation paradigms including paired-pulse stimulation. Genetic depletion of K<sub>v</sub>β1 blocked all broadening of the AP<sub>syn</sub> during high-frequency stimulation and eliminated synaptic facilitation without altering the initial probability of vesicle release. Thus, using all quantitative optical measurements of presynaptic physiology, we reveal a critical role for presynaptic K<sub>v</sub> channels in synaptic facilitation at presynaptic terminals of the hippocampus upstream of the exocytic machinery.","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Nov","modification":"2025-04-21T18:02:04.117Z","creation":"2025-04-05T17:02:23.307Z"},"accession":"S-EPMC7703594","cross_references":{"pubmed":["33168717"],"doi":["10.1073/pnas.2000790117"]}}