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Inhibition of evoked acetylcholine release: two different mechanisms in the Torpedo electric organ

Loctin, F.
Published in European Journal of Pharmacology. 1987, vol. 133, no. 2, p. 225-234
Abstract The action of agents inhibiting evoked transmitter release was investigated by analysing the Ca2+ secretion relationship, electrophysiologically and biochemically, and by measuring the stimulation-induced 45Ca accumulation in the tissue. Transmitter release saturated at external Ca2+ concentrations higher than 4 mM, the releasing mechanism probably being the limiting step. Antagonists of Ca2+ entry (Mg2+, Cd2+, diltiazem) decreased the sensitivity of acetylcholine release to Ca2+, acting as competitive inhibitors, and reduced the stimulation-induced 45Ca accumulation. Quinacrine produced similar effects, indicating that it interacts primarily with Ca2+ entry. In contrast, oxotremorine and adenosine depressed transmitter release proportionally at all Ca2+ concentrations, acting as non-competitive inhibitors, and did not modify the stimulation-induced 45Ca accumulation. Their inhibitory effects were additive and reflected a decrease in the quantal content of the responses evoked. It is concluded that both drugs inhibit cholinergic transmission in the electric organ without altering Ca2+ entry into the nerve endings.
Keywords Acetylcholine/ secretionAdenosine/pharmacologyAnimalsCalcium/ metabolismCalcium Channel Blockers/pharmacologyElectric Organ/ drug effects/innervation/metabolismElectric StimulationIon Channels/ drug effects/physiologyMagnesium/pharmacologyOxotremorine/pharmacologyQuinacrine/pharmacologyTorpedo
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PMID: 2434349

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Deposited on : 2010-08-06

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