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Calcium‐induced calcium increase in secretory vesicles of permeabilized rat neurohypophysial nerve terminals
Author(s) -
Troadec JeanDenis,
Thirion Sylvie,
Laugier JeanPierre,
Nicaise Ghislain
Publication year - 1998
Publication title -
biology of the cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 85
eISSN - 1768-322X
pISSN - 0248-4900
DOI - 10.1111/j.1768-322x.1998.tb01043.x
Subject(s) - ruthenium red , organelle , calcium , vesicle , biology , secretory vesicle , digitonin , secretion , biophysics , microbiology and biotechnology , biochemistry , sodium , chemistry , membrane , organic chemistry
Digitonin‐permeabilized isolated neurohypophysial nerve terminals are known to release their secretory vesicle content under calcium challenge. On this preparation, we monitored intra‐organelle Ca 2+ concentration using digital fluorescence microscopy of Fura‐2. The superfusion of artificial intracellular solution containing 10 to 50 μM Ca 2+ induced an intra‐organelle [Ca 2+ ] increase. Two major organelles are candidates for this increase: secretory vesicles and mitochondria. In an attempt to detect calcium changes in the vesicles, ruthenium red was used to impair mitochondrial calcium uptake. Part of the ruthenium red‐insensitive intra‐organelle [Ca 2+ ] increase was abolished by raising sodium in the solution. Removing sodium boosted the intra‐organelle [Ca 2+ ] increase. These results taken together suggest the participation of Na/Ca exchange, known to exist in the membrane of these secretory vesicles. In addition to Na/Ca exchange, there would be at least another mechanism of vesicular calcium intake, as suggested by the partial inhibition of intra‐organelle [Ca 2+ ] increase obtained under acidic compartments: neutralization with NH 4 Cl. This mechanism remains to be defined. The main conclusion presented here, that an intravesicular [Ca 2+ ] increase takes place at the rate of secretion, was predicted by the hypothesis that intravesicular Ca 2+ changes would be involved in stimulus‐secretion coupling.