Smith P A, Zidichouski J A
Br J Pharmacol. 1985 Jan;84(1):221-5.
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.
采用蔗糖间隙技术，从两栖类交感神经节的神经元记录肾上腺素诱导的超极化（AdH）以及毒蕈碱和促黄体生成素释放激素（LHRH）所诱发的反应。当通过LHRH或毒蕈碱的灌流促进“M通道”关闭时，AdH的幅度降低。4-氨基吡啶（4-AP，1 mM）拮抗AdH，但不拮抗毒蕈碱激动剂诱发的去极化。这意味着参与AdH电发生的通道具有与“M通道”不同的药理学特性，并且AdH不是由“M通道”在其正常电压范围之外的开放所产生的。毒蕈碱和LHRH使AdH衰减的可能解释可能是：（i）这些物质产生的细胞内生化变化以某种方式干扰了AdH的产生，或者（ii）毒蕈碱和LHRH与介导AdH的肾上腺素能受体具有变构相互作用。
