1. A grease gap d.c. recording technique was used to measure electrophysiological responses of the isolated rat superior cervical ganglion. 2. Adenosine at 100 microM depressed depolarisations to the muscarinic agonists carbachol, muscarine and methylfurmethide. In contrast adenosine (100 microM) did not alter depolarisations to 1,1-dimethyl-4-phenylpiperazinium, 2-methyl-5-hydroxytryptamine and potassium and enhanced depolarisations to 5-hydroxytryptamine and gamma-aminobutyric acid. 3. Adenosine-induced depressions of the depolarisations to carbachol, muscarine, and methylfurmethide tended to be increased in the presence of 0.3 microM methoctramine (a muscarinic receptor antagonist with slight selectivity for M2 receptors). The increase was statistically significant (P < 0.01) for carbachol. 4. Medium containing 0.1 mM Ca2+ and 0.3 microM pirenzepine augmented the hyperpolarising phase of the response to carbachol. Adenosine (10-300 microM) hyperpolarised ganglia and did not significantly alter the hyperpolarisation to 0.3 or 1 microM carbachol but selectively reduced the depolarisation response to 3 microM carbachol. 5. Adenosine-induced hyperpolarisations (100 microM) were enhanced when applied during depolarisations to muscarinic agonists (muscarine, pilocarpine, N-methyl-N-(l-methyl-4-pyrrolidine-2-butynyl)acetamide (BM-5)), and other M-current inhibitors, barium and eledoisin-related-peptide. Adenosine induced hyperpolarisations were not affected by D-Ala6-luteinizing-hormone-releasing-hormone or uridine 5'-triphosphate which produced small depolarisations. 6. It is concluded that adenosine acts selectively in opposing mechanisms of depolarisation of the rat SCG that are due to the action of muscarinic agonists (acting via M1-receptors) and by other M-current inhibitors.