The aim of our study was to analyse drug-induced decremental oscillations following spike potential evoked by a preganglionic stimulus in the superior cervical ganglion of the cat in situ. Ganglionic compound action potentials evoked by preganglionic stimulation and postganglionic asynchronous discharge induced by drugs injected into the ganglionic vascular bed were registered. The muscarine like drugs 4-( m-chlorophenylcarbamoyloxy)-2-butynyl trimethylammonium chloride (McN-A-343), N-benzyl-3-pyrrolidyl acetate methobromide (AHR-602), and pilocarpine, and histamine and bradykinin induced decremental oscillations following spike potential occurring at the time of the late negative wave onset. These drugs evoked slowly developing asynchronous discharge of low amplitude; time of onset and duration of asynchronous discharge and of decremental oscillations were similar. Atropine, which decreases late negative wave amplitude, depressed decremental oscillations induced by McN-A-343, however it did not inhibit histamine-induced decremental oscillations. The ganglion-depolarizing drug isoprenaline, which does not induce asynchronous discharge, evoked increase in the late negative wave amplitude without decremental oscillations. Nicotine induced decrease in the late negative wave amplitude with no concomitant decremental oscillations. Our results indicate that drugs inducing decremental oscillations following spike potential have the common characteristic of causing asynchronous discharge by stimulation of non-nicotinic receptor sites in the cat superior cervical ganglion. It is suggested that a process closely related to the stimulus-evoked release of acetylcholine from presynaptic endings is responsible for the appearance of decremental oscillations by modulating the discharge originating at non-nicotinic receptor sites.