Alpha 2-adrenergic hyperpolarization is not involved in slow synaptic inhibition in amphibian sympathetic ganglia.

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. Desmethylimipramine (DMI, 0.5 microM) lowered the EC50 for adrenaline from 1.65 microM (1.23-2.21 microM, n = 10) to 0.30 microM (0.21-0.41 microM, n = 8). DMI did not potentiate the slow i.p.s.p. or the MChH. Propranolol, sotalol or prazosin (1 microM) did not antagonize the AdH. The response was antagonised by phentolamine (IC50 = 0.53 microM), yohimbine (IC50 = 6.2 nM) and idazoxan (IC50 = 0.59 microM). Yohimbine (0.1 microM) did not reduce the amplitude of the slow i.p.s.p. or the MChH. The slow i.p.s.p. was eliminated in Ringer solution containing Cd2+ (100 microM). This concentration of Cd2+ did not reduce the amplitude of the MChH. Alpha-Methylnoradrenaline produced a concentration-dependent hyperpolarization with an EC50 of 0.31 microM (0.13-0.73 microM, n = 5), in the presence of DMI (0.5 microM). 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.