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dc.contributor.authorYin, Yong
dc.contributor.authorDayanithi, Govindan
dc.contributor.authorLemos, Jose R.
dc.date2022-08-11T08:09:34.000
dc.date.accessioned2022-08-23T16:35:43Z
dc.date.available2022-08-23T16:35:43Z
dc.date.issued2002-03-08
dc.date.submitted2009-03-26
dc.identifier.citation<p>J Physiol. 2002 Mar 1;539(Pt 2):409-18.</p>
dc.identifier.issn0022-3751 (Print)
dc.identifier.pmid11882674
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38625
dc.description.abstractIon channels from bovine neurohypophysial secretory granules (NSG) were incorporated into artificial lipid bilayers. Specific antibodies against identified synaptic vesicle proteins were tested on such incorporated channel activity and on peptide release from rat permeabilized neurohypophysial terminals. Both the NSG cation channel and Ca(2+)-dependent release were inhibited by only SY-38, a monoclonal antibody directed against the C-terminus of synaptophysin. SY-38 and Ca(2+) altered both the gating and conductance of the NSG cation channel, but in opposite ways. The close correlation between SY-38 effects on Ca(2+)-dependent channel activity and release leads us to conclude that this synaptophysin-like NSG channel is directly involved in peptide secretion from these central nervous system terminals.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=11882674&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2290157/
dc.subjectAnimals
dc.subjectArginine Vasopressin
dc.subjectCalcium
dc.subjectCattle
dc.subjectCytoplasmic Granules
dc.subjectElectrophoresis, Polyacrylamide Gel
dc.subjectElectrophysiology
dc.subjectImmunoblotting
dc.subjectIon Channels
dc.subjectLipid Bilayers
dc.subjectLiposomes
dc.subjectMembrane Proteins
dc.subjectNeurosecretory Systems
dc.subjectPatch-Clamp Techniques
dc.subjectPituitary Gland, Posterior
dc.subjectPresynaptic Terminals
dc.subjectSynaptic Vesicles
dc.subjectSynaptophysin
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleCa(2+)-regulated, neurosecretory granule channel involved in release from neurohypophysial terminals
dc.typeJournal Article
dc.source.journaltitleThe Journal of physiology
dc.source.volume539
dc.source.issuePt 2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1487
dc.identifier.contextkey798462
html.description.abstract<p>Ion channels from bovine neurohypophysial secretory granules (NSG) were incorporated into artificial lipid bilayers. Specific antibodies against identified synaptic vesicle proteins were tested on such incorporated channel activity and on peptide release from rat permeabilized neurohypophysial terminals. Both the NSG cation channel and Ca(2+)-dependent release were inhibited by only SY-38, a monoclonal antibody directed against the C-terminus of synaptophysin. SY-38 and Ca(2+) altered both the gating and conductance of the NSG cation channel, but in opposite ways. The close correlation between SY-38 effects on Ca(2+)-dependent channel activity and release leads us to conclude that this synaptophysin-like NSG channel is directly involved in peptide secretion from these central nervous system terminals.</p>
dc.identifier.submissionpathoapubs/1487
dc.contributor.departmentProgram in Neuroscience
dc.contributor.departmentDepartment of Physiology
dc.source.pages409-18


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