ADENOSINE SELECTIVELY DEPRESSES MUSCARINIC COMPARED WITH NONMUSCARINIC RECEPTOR-MEDIATED DEPOLARIZATION OF THE RAT SUPERIOR CERVICAL-GANGLION

1. A grease gap d.c, recording technique was used to measure electroph ysiological responses of the isolated rat superior cervical ganglion. 2. Adenosine at 100 mu M depressed depolarisations to the muscarinic a gonists carbachol, muscarine and methylfurmethide. In contrast adenosi ne (100 mu M) did not alter depolarisations to 1,1-dimethyl-4-phenylpi perazinium, 2-methyl-5-hydroxytryptamine and potassium and enhanced de polarisations to 5-hydroxytryptamine and gamma-aminobutyric acid. 3. A denosine-induced depressions of the depolarisations to carbachol, musc arine, and methylfurmethide tended to be increased in the presence of 0.3 mu M methoctramine (a muscarinic receptor antagonist with slight s electivity for M(2) receptors). The increase was statistically signifi cant (P < 0.01) for carbachol. 4. Medium containing 0.1 mM Ca2+ and 0. 3 mu M pirenzepine augmented the hyperpolarising phase of the response to carbachol. Adenosine (10-300 mu M) hyperpolarised ganglia and did not significantly alter the hyperpolarisation to 0.3 or 1 mu M carbach ol but selectively reduced the depolarisation response to 3 mu M carba chol. 5. Adenosine-induced hyperpolarisations (100 mu M) were enhanced when applied during depolarisations to muscarinic agonists (muscarine , pilocarpine, thyl-N-(1-methyl-4-pyrrolidine-2-butynyl)acetamide (BM- 5)), and other M-current inhibitors, barium and eledoisin-related-pept ide. Adenosine induced hyperpolarisations were not affected by D-Ala(6 )-luteinizing-hormone-releasing-hormone or uridine 5'-triphosphate whi ch produced small depolarisations. 6. It is concluded that adenosine a cts selectively in opposing mechanisms of depolarisation of the rat SC G that are due to the action of muscarinic agonists (acting via M(1)-r eceptors) and by other M-current inhibitors.