Sodium-dependent efflux of [3H]GABA from synaptosomes probably related to mitochondrial calcium mobilization.


It has been suggested that mitochondria might modify transmitter release through the control of intracellular Ca2+ levels. Treatments known to inhibit Ca2+ retention by mitochondria lead to an increased transmitter liberation in the absence of external Ca2+, both at the frog neuromuscular junction and from isolated nerve endings. Sodium ions stimulate Ca2… (More)


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