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    Ca(2+)-regulated, neurosecretory granule channel involved in release from neurohypophysial terminals

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    Authors
    Yin, Yong
    Dayanithi, Govindan
    Lemos, Jose R.
    UMass Chan Affiliations
    Program in Neuroscience
    Department of Physiology
    Document Type
    Journal Article
    Publication Date
    2002-03-08
    Keywords
    Animals
    Arginine Vasopressin
    Calcium
    Cattle
    Cytoplasmic Granules
    Electrophoresis, Polyacrylamide Gel
    Electrophysiology
    Immunoblotting
    Ion Channels
    Lipid Bilayers
    Liposomes
    Membrane Proteins
    Neurosecretory Systems
    Patch-Clamp Techniques
    Pituitary Gland, Posterior
    Presynaptic Terminals
    Synaptic Vesicles
    Synaptophysin
    Life Sciences
    Medicine and Health Sciences
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    Link to Full Text
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2290157/
    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.
    Source

    J Physiol. 2002 Mar 1;539(Pt 2):409-18.

    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/38625
    PubMed ID
    11882674
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