ArticleThe Journal of physiology2002
Ca(2+)-regulated, neurosecretory granule channel involved in release from neurohypophysial terminals.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Room for Two: The Synaptophysin/Synaptobrevin Complex.Frontiers in synaptic neuroscience · 2021Article
- AVP modulation of the vestibular nucleus via V1b receptors potentially contributes to the development of motion sickness in rat.Molecular brain · 2015Article
- Functional ryanodine receptors in the membranes of neurohypophysial secretory granules.The Journal of general physiology · 2014Article
- The Sybtraps: control of synaptobrevin traffic by synaptophysin, α-synuclein and AP-180.Traffic (Copenhagen, Denmark) · 2014Review
- The association of dynamin with synaptophysin regulates quantal size and duration of exocytotic events in chromaffin cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Exocytotic catecholamine release is not associated with cation flux through channels in the vesicle membrane but Na+ influx through the fusion pore.Nature cell biology · 2007Article
- The synaptic vesicle protein synaptophysin: purification and characterization of its channel activity.Biophysical journal · 2002Article
- Synaptophysins: vesicular cation channels?The Journal of physiology · 2002Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.