α ₂‐Adrenergic hyperpolarization is not involved in slow synaptic inhibition in amphibian sympathetic ganglia

The adrenaline‐induced hyperpolarization (Ad_H), slow inhibitory postsynaptic potential (slow i.p.s.p.) and hyperpolarizing phase of the response to methacholine (MCh_H) in Rana pipiens sympathetic ganglia were studied by means of the sucrose‐gap technique. 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 MCh_H. Propranolol, sotalol or prazosin (1 μM) did not antagonize the Ad_H. 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 MCh_H. 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 MCh_H. 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). These results are consistent with the hypothesis that the Ad_H 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. 1986 British Pharmacological Society