α2-Adrenergic hyperpolarization is not involved in slow synaptic inhibition in amphibian sympathetic ganglia

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Abstract
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 μM) lowered the EC50 for adrenaline from 1.65 μM (1.23–2.21 μM, n = 10) to 0.30 μM (0.21–0.41 μM, n = 8). DMI did not potentiate the slow i.p.s.p. or the MChH. 3 Propranolol, sotalol or prazosin (1 μM) did not antagonize the AdH. The response was antagonised by phentolamine (IC50 = 0.53 μM), yohimbine (IC50 = 6.2 nM) and idazoxan (IC50 = 0.59 μM). Yohimbine (0.1 μM) 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 μM): This concentration of Cd2+ did not reduce the amplitude of the MChH. 5 α-Methylnoradrenaline produced a concentration-dependent hyperpolarization with an EC50 of 0.31 μM (0.13–0.73 μM, n = 5), in the presence of DMI (0.5 μM). 6 These results are consistent with the hypothesis that the AdH may be generated by activation of a receptor similar to the mammalian α2-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.