Desensitization of the muscarinic receptor controlling action potential of bullfrog atrial muscles.

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Abstract
Action potentials of the bullfrog atrial muscle being depressed by carbachol in concentrations of (1-5) .times. 10-7 M showed a slow recovery when application of the drug was sustained. The rate of onset of recovery largely varied depending on individual preparations. The recovery of action potentials was neither due to changes in the ionic distribution across the membrane nor to a secondary action of catecholamine which was released by the nicotinic action of carbachol on sympathetic nerve terminals. The muscarinic ACh [acetylcholine] receptor responsible for the depression of action potentials showed desensitization to the action of its agonist. The slow inward current recorded by the voltage-clamp experiment showed a decrease and subsequent slow recovery in the presence of carbachol. The muscarinic ACh receptor associating with the ionic channel of the slow inward current apparently showed desensitization. The muscarinic ACh receptor of bullfrog atrial muscle may compose a receptor-ionic channel complex (RICC) with voltage-dependent Ca2+ channel and the molecular reaction between this RICC and agonist may be comparable to that occurring in the nicotinic RICC of the frog end-plate.