Morot-Gaudry_1984_Neurochem.Int_6_553

The effects of trimethyl-tin (anion-hydroxyde ionophore, inhibiting oxydative phosphorylation and H(+)-ATPase) probenecid (inhibitor of anion transport in neural cells) and phenylglyoxal (arginine-specific reagent, inhibiting chloride exchanges in erythrocytes) were examined in Torpedo synaptosomes prepared from electric organ. All drugs significantly reduced the stimulated release of acetylcholine triggered by depolarization of nerve endings with high-K(+) and/or gramicidin D. In contrast, trimethyl-tin, probenecid and phenylglyoxal did not affect the ionophore A23187-induced release of acetylcholine from the synaptosomes. The inhibitory potency of the compound trimethyl-tin was found to be similar to that of probenecid and phenylglyoxal on depolarization-induced acetylcholine release. This leads us to suggest that a relationship exists between modification of anion distribution during depolarization and acetylcholine release process. Moreover, since the release of ACh by calcium-ionophore A23187 was unaffected by trimethyl-tin, probenecid or phenylglyoxal, such compounds may also have an action on voltage-dependent Ca(2+) flux across presynaptic membrane.