Muscarine and luteinizing hormone releasing hormone attenuate adrenaline induced hyperpolarization in amphibian sympathetic ganglia.

The adrenaline-induced hyperpolarization (AdH) and the responses evoked by muscarine and luteinizing hormone releasing hormone (LHRH) were recorded from neurones in amphibian sympathetic ganglia by means of the sucrose gap technique. The amplitude of the AdH was reduced when 'M-channel' closure was promoted by superfusion of LHRH or muscarine. 4-Aminopyridine (4-AP, 1 mM) antagonized the AdH, but not the depolarization evoked by muscarinic agonists. This implies that the channels involved in the electrogenesis of the AdH have different pharmacological properties from 'M-channels' and that the AdH is not generated by the opening of 'M-channels' outside their normal voltage range. Possible explanations for the attenuation of the AdH by muscarine and LHRH might be that (i) intracellular biochemical changes produced by these substances somehow interfere with the generation of the AdH or that (ii) muscarine and LHRH have allosteric interactions with the adrenoceptor mediating the AdH.