Action of exogenic acetylcholine on the potassium currents of frog motor nerve endings

Abstract

Using nerve-muscle preparations of the cutaneous pectoris muscle of the frog, and recording extracellular evoked electrical responses from a nerve ending (NE), we have studied the mechanisms by which exogenic acetylcholine (ACh) influences the ion currents of a motor nerve ending. We have established that ACh in concentrations of 0.1–0.6 mmoles/liter causes an increase in the third phase of the NE response, and in concentrations of 0.7–2.0 mmoles/liter, suppresses it. We have found that tubocurarine and atropine do not block the effects of ACh. It has been shown that the ACh-induced increase in the amplitude of the third phase of the NE response is seen against a background of calcium channel blockers, and it can be eliminated by 4-aminopyridine (4-AP) and tetraethylammonium. The inhibitory effect of ACh on the third phase of the NE response is not present in calcium-free solutions, nor when the calcium current is blocked. A discussion is given of the mechanisms of exogenic and endogenic ACh action on the potential-dependent and calcium-activated potassium current of the NE.