ALPHA-2-ADRENERGIC HYPERPOLARIZATION IS NOT INVOLVED IN SLOW SYNAPTIC INHIBITION IN AMPHIBIAN SYMPATHETIC-GANGLIA

1. The adrenaline-induced hyperpolarization (AdH), slow inhibitory postsynaptic potential (slow i.p.s.p.) and hyperpolarizing phase of the response to methacholine (MChH) in Rana pipiens sympathetic ganglia were studied by means of the sucrose-gap technique. 2. Desmethylimipramine (DMI, 0.5 .mu.M) lowered the EC50 for adrenaline from 1.65 .mu.M (1.23-2.21 .mu.M, n = 10) to 0.30 .mu.M (0.21-0.41 .mu.M, n = 8). DMI did not potentiate the slow i.p.s.p. or the MChH. 3. Propranolol, sotalol or prazosin (1 .mu.M) did not antagonize the AdH. The response was antagonized by phentolamine (IC50 = 0.53 .mu.M), yohimbine (IC50 = 6.2 nM) and idazoxan (IC50 = 0.59 .mu.M). Yohimbine (0.1 .mu.M) did not reduce the amplitude of the slow i.p.s.p. or the MChH. 4. The slow i.p.s.p. was eliminated in Ringer solution containing Cd2+ (100 .mu.M). This concentration of Cd2+ did not reduce the amplitude of the MChH. 5. .alpha.-Methylnoradrenaline produced a concentration-dependent hyperpolarization with an EC50 of 0.31 .mu.M (0.13-0.73 .mu.M, n = 5), in the presence of DMI (0.5 .mu.M). 6. These results are consistent with the hypothesis that the AdH may be generated by activation of a receptor similar to the mammalian .alpha.2-adrenoceptor. No evidence was found in support of the hypothesis that an adrenergic interneurone is involved in the synaptic pathway for the slow i.p.s.p.