Sucrose gap recording technique was employed to record surface potentials from superior cervical ganglia (SCGs) of several species. Repetitive preganglionic stimulation (30 Hz, 1-2 sec) elicited in curarized rabbit, rat and cat SCGs, a biphasic response as the initial slow positive (P) potential, was followed by a late negative (LN) potential. In curarized guinea-pig SCG, a LN response with no detectable P potential was observed. Neostigmine (0.5-1 microM) increased the amplitude and duration of the P and LN responses in the majority of the rabbit, rat and cat SCGs. LN response of guinea-pig SCG was first enhanced by neostigmine; subsequently, it was converted into a hyperpolarizing potential. Alpha receptor antagonists, phenoxybenzamine, phentolamine and dihydroergotamine, and a beta receptor antagonist, propranolol, did not appreciably alter the P and LN responses of the rabbit, cat and rat SCG or neostigmine-induced hyperpolarization of the guinea-pig SCG. Dopaminergic receptor antagonists, haloperidol, chlorpromazine and metoclopramide, caused no significant depression of the P and LN responses in the rabbit SCG. Atropine (1 microM) consistently abolished the P and/or LN of all these ganglia, as well as the neostigmine-induced hyperpolarization of the guinea-pig SCG. These results demonstrate that muscarinic receptors are involved in the generation of P and LN potentials of mammalian sympathetic ganglia, while the adrenergic and disynaptic nature of P response remains to be clarified. Furthermore, there appears to be no correlation between the generation of P potential and elevation of cyclic AMP in the SCG.