Abstract

Muscarine and oxotremorine caused postganglionic firing that was blocked by atropine. The surface potential evoked by muscarine and oxotremorine was biphasic and consisted of hyperpolarization followed by depolarization. Blockade of transmission by the drugs occurred during hyperpolarization and was characterized by an increase in the negative afterpotential. The synaptic potential was depressed by muscarine and oxotremorine. The relationship between drug-induced hyperpolarization and ganglion blockade was questioned. Oxotremorine caused a persistent depolarization of the ganglion (several hours). The actions of muscarine and oxotremorine are qualitatively similar to those of methacholine. N-benzyl-3-pyrrolidyl acetate methobromide (AHR-602) caused atropine-sensitive ganglionic firing and a monophasic surface depolarization that was unaffected by atropine. Ganglionic blockade by AHR-602 occurred during the depolarization, was unaffected by atropine, was antagonized by tetanic stimulation and was independent of frequency of preganglionic stimulation. The blocking actions of AHR-602 are similar to those of 4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium chloride. It is unlikely that the block of transmission by AHR-602 was related to ganglionic depolarization.