Ca(2+)-regulated, neurosecretory granule channel involved in release from neurohypophysial terminals
dc.contributor.author | Yin, Yong | |
dc.contributor.author | Dayanithi, Govindan | |
dc.contributor.author | Lemos, Jose R. | |
dc.date | 2022-08-11T08:09:34.000 | |
dc.date.accessioned | 2022-08-23T16:35:43Z | |
dc.date.available | 2022-08-23T16:35:43Z | |
dc.date.issued | 2002-03-08 | |
dc.date.submitted | 2009-03-26 | |
dc.identifier.citation | <p>J Physiol. 2002 Mar 1;539(Pt 2):409-18.</p> | |
dc.identifier.issn | 0022-3751 (Print) | |
dc.identifier.pmid | 11882674 | |
dc.identifier.uri | http://hdl.handle.net/20.500.14038/38625 | |
dc.description.abstract | 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. | |
dc.language.iso | en_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.url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2290157/ | |
dc.subject | Animals | |
dc.subject | Arginine Vasopressin | |
dc.subject | Calcium | |
dc.subject | Cattle | |
dc.subject | Cytoplasmic Granules | |
dc.subject | Electrophoresis, Polyacrylamide Gel | |
dc.subject | Electrophysiology | |
dc.subject | Immunoblotting | |
dc.subject | Ion Channels | |
dc.subject | Lipid Bilayers | |
dc.subject | Liposomes | |
dc.subject | Membrane Proteins | |
dc.subject | Neurosecretory Systems | |
dc.subject | Patch-Clamp Techniques | |
dc.subject | Pituitary Gland, Posterior | |
dc.subject | Presynaptic Terminals | |
dc.subject | Synaptic Vesicles | |
dc.subject | Synaptophysin | |
dc.subject | Life Sciences | |
dc.subject | Medicine and Health Sciences | |
dc.title | Ca(2+)-regulated, neurosecretory granule channel involved in release from neurohypophysial terminals | |
dc.type | Journal Article | |
dc.source.journaltitle | The Journal of physiology | |
dc.source.volume | 539 | |
dc.source.issue | Pt 2 | |
dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/oapubs/1487 | |
dc.identifier.contextkey | 798462 | |
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.submissionpath | oapubs/1487 | |
dc.contributor.department | Program in Neuroscience | |
dc.contributor.department | Department of Physiology | |
dc.source.pages | 409-18 |