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Regulation of cytosolic calcium concentration in presynaptic nerve endings isolated from rat brain.
Author(s) -
Nachshen D A
Publication year - 1985
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1985.sp015697
Subject(s) - chemistry , biophysics , cytosol , calcium , free nerve ending , valinomycin , synaptosome , biochemistry , membrane potential , endocrinology , biology , enzyme , organic chemistry
The regulation of cytosolic Ca concentration ([Ca]i) was studied with the fluorescent Ca indicator, quin2, in pinched‐off presynaptic nerve endings (synaptosomes) isolated from rat brain. The resting [Ca]i is 0.1‐0.2 microM, in solutions containing 1‐2 mM‐Ca. [Ca]i increases by only 100‐150 nM when the external Ca concentration is increased from 0.02 to 2 mM. The mitochondrial inhibitors valinomycin and fluoro‐carbonyl cyanide phenylhydrazone (FCCP) increase [Ca]i by 100‐200 nM. This increase is not correlated with the resting level of [Ca]i prior to the addition of inhibitors, but it is dependent on the presence of external Ca. It seems likely that the effect of these inhibitors on [Ca]i is a secondary consequence of metabolic inhibition. [Ca]i increases by about 2‐fold when the external Na concentration is lowered from 145 to 5 mM, and returns to its initial level when external Na is restored. This recovery occurs also in the presence of FCCP. These results suggest that Na/Ca exchange, but not mitochondrial Ca uptake, plays a role in regulating [Ca]i and in allowing the nerve terminals to recover from Ca loading.