{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Brackenbury WJ"],"funding":["NIMH NIH HHS","NINDS NIH HHS"],"pagination":["2283-8"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2836661"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["107(5)"],"pubmed_abstract":["Voltage-gated Na(+) channel (VGSC) beta1 subunits regulate cell-cell adhesion and channel activity in vitro. We previously showed that beta1 promotes neurite outgrowth in cerebellar granule neurons (CGNs) via homophilic cell adhesion, fyn kinase, and contactin. Here we demonstrate that beta1-mediated neurite outgrowth requires Na(+) current (I(Na)) mediated by Na(v)1.6. In addition, beta1 is required for high-frequency action potential firing. Transient I(Na) is unchanged in Scn1b (beta1) null CGNs; however, the resurgent I(Na), thought to underlie high-frequency firing in Na(v)1.6-expressing cerebellar neurons, is reduced. The proportion of axon initial segments (AIS) expressing Na(v)1.6 is reduced in Scn1b null cerebellar neurons. In place of Na(v)1.6 at the AIS, we observed an increase "],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Functional reciprocity between Na+ channel Nav1.6 and beta1 subunits in the coordinated regulation of excitability and neurite outgrowth."],"pmcid":["PMC2836661"],"funding_grant_id":["R01 NS076752","R01 NS038297","R01 MH059980","R01 NS38297"],"pubmed_authors":["Nukina N","Oyama F","Ranscht B","Brackenbury WJ","Calhoun JD","Miyazaki H","Isom LL","Chen C"],"additional_accession":[]},"is_claimable":false,"name":"Functional reciprocity between Na+ channel Nav1.6 and beta1 subunits in the coordinated regulation of excitability and neurite outgrowth.","description":"Voltage-gated Na(+) channel (VGSC) beta1 subunits regulate cell-cell adhesion and channel activity in vitro. We previously showed that beta1 promotes neurite outgrowth in cerebellar granule neurons (CGNs) via homophilic cell adhesion, fyn kinase, and contactin. Here we demonstrate that beta1-mediated neurite outgrowth requires Na(+) current (I(Na)) mediated by Na(v)1.6. In addition, beta1 is required for high-frequency action potential firing. Transient I(Na) is unchanged in Scn1b (beta1) null CGNs; however, the resurgent I(Na), thought to underlie high-frequency firing in Na(v)1.6-expressing cerebellar neurons, is reduced. The proportion of axon initial segments (AIS) expressing Na(v)1.6 is reduced in Scn1b null cerebellar neurons. In place of Na(v)1.6 at the AIS, we observed an increase ","dates":{"release":"2010-01-01T00:00:00Z","publication":"2010 Feb","modification":"2025-04-26T12:30:49.1Z","creation":"2019-03-27T00:29:16Z"},"accession":"S-EPMC2836661","cross_references":{"pubmed":["20133873"],"doi":["10.1073/pnas.0909434107"]}}