Role of synaptosomal Na-accumulation in transmitter release.
The mechanism whereby Na+, K+-ATPase inhibitors such as ouabain trigger transmitter release in a calcium-independent manner remains obscure. We have examined the possible role of intra-synaptosomal sodium ion accumulation in ouabain-induced acetylcholine (ACh) release by: 1) Measuring 22Na accumulation in cat cortical synaptosomes in the presence of ouabain, A23187, veratridine, or strophanthidin over the same time course in which we previously determined their effects on ACh release; and 2) measuring synaptosomal 22Na accumulation and ACh-release in the presence of ouabain plus tetrodotoxin in normal or calcium-free buffer. Our results indicate that tetrodotoxin-dependent 22Na accumulation is at least partially responsible for ouabain-induced ACh release in normal and calcium-free media, but that this ion-accumulation per se is not sufficient to elicit release with other secretogogues.
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002540:Cerebral Cortex / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D010042:Ouabain / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000378:metabolism*; D013327:Strophanthidin / Q000494:pharmacology; D013574:Synaptosomes / Q000378:metabolism*; D013779:Tetrodotoxin / Q000494:pharmacology; D014701:Veratridine / Q000494:pharmacology
D000001:Calcimycin; D013779:Tetrodotoxin; D010042:Ouabain; D013327:Strophanthidin; D014701:Veratridine; D012964:Sodium; D000109:Acetylcholine