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J Physiol Volume 539, Number 2, 409-418, March 1, 2002 DOI: 10.1113/jphysiol.2002.012943
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Journal of Physiology (2002), 539.2, pp. 409-418
© Copyright 2002 The Physiological Society
DOI: 10.1113/jphysiol.2001.012943

Ca2+-regulated, neurosecretory granule channel involved in release from neurohypophysial terminals

Yong Yin, Govindan Dayanithi* and José R. Lemos

Department of Physiology and Program in Neuroscience, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA and *INSERM-U432, University of Montpellier II, F-34095, Montpellier, France

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 Ca2+-dependent release were inhibited by only SY-38, a monoclonal antibody directed against the C-terminus of synaptophysin. SY-38 and Ca2+ altered both the gating and conductance of the NSG cation channel, but in opposite ways. The close correlation between SY-38 effects on Ca2+-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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D. Gincel and V. Shoshan-Barmatz
The Synaptic Vesicle Protein Synaptophysin: Purification and Characterization of Its Channel Activity
Biophys. J., December 1, 2002; 83(6): 3223 - 3229.
[Abstract] [Full Text] [PDF]




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