Inhibition of evoked acetylcholine release: two different mechanisms in the Torpedo electric organ
|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/ secretion — Adenosine/pharmacology — Animals — Calcium/ metabolism — Calcium Channel Blockers/pharmacology — Electric Organ/ drug effects/innervation/metabolism — Electric Stimulation — Ion Channels/ drug effects/physiology — Magnesium/pharmacology — Oxotremorine/pharmacology — Quinacrine/pharmacology — Torpedo|
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