Studies on the relationship between Ca2+ efflux from mitochondria and the release of amino acid neurotransmitters.
It is known that transmitter release depends upon the entry of calcium ions into the synaptic terminal. Mitochondria have been suggested to play a key role on the regulation of intracellular Ca2+ concentration, thereby influencing transmitter liberation and synaptic transmission. Here we report the stimulatory effect of DNP and FCCP, uncouplers of oxidative phosphorylation, and quinidine, known to induce muscle contractures and increase Ca2+ efflux from muscle mitochondria, on both [14C]glutamic acid and [3H]GABA unstimulated release from synaptosomes and loss of 45Ca2+ from preloaded whole brain mitochondria. Results showed that the spontaneous efflux of non-putative neurotransmitters, leucine and alpha-aminoisobutyric acid, was less affected or not stimulated at all, under similar experimental conditions. Data suggest that calcium ions released from mitochondria are able to trigger neurotransmitter release.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002259:Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone / Q000494:pharmacology; D004140:Dinitrophenols / Q000494:pharmacology; D005971:Glutamates / Q000378:metabolism*; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D011802:Quinidine / Q000494:pharmacology; D051381:Rats; D013574:Synaptosomes / Q000187:drug effects / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D004140:Dinitrophenols; D005971:Glutamates; D002259:Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone; D005680:gamma-Aminobutyric Acid; D011802:Quinidine; D002118:Calcium