Hanani M, Wood J D
Department of Physiology, College of Medicine, Ohio State University, Columbus 43210.
Eur J Pharmacol. 1992 Jan 28;211(1):23-7. doi: 10.1016/0014-2999(92)90256-4.
The electrophysiological actions of corticotropin-releasing hormone (CRH) on myenteric neurons from the guinea-pig ileum were studied by intracellular microelectrode recording. CRH, when applied by micropressure ejection or in the medium (0.2-20 nM) evoked prolonged depolarization in 21 of 42 S/type 1 neurons and in 28 of 40 AH/type 2 neurons. These responses were associated with increased input resistance and augmented excitability. The post-spike hyperpolarization in AH/type 2 cells was suppressed during the CRH-evoked responses. The reversal potential of the response to CRH was about -90 mV, consistent with the closure of potassium channels by the peptide. The CRH-induced depolarization was prevented by incubation in 10 microM 5'-N-ethylcarboxamidoadenosine (NECA, an adenosine analog) suggesting that the response was mediated by stimulation of adenylate cyclase and elevation of cAMP. CRH reduced the amplitude of fast nicotinic excitatory postsynaptic potentials. This appeared to be a postsynaptic action because the peptide also reduced the responses to exogenously applied acetylcholine. These results suggest that CRH can directly influence intestinal function by acting on myenteric neurons.
采用细胞内微电极记录法，研究了促肾上腺皮质激素释放激素（CRH）对豚鼠回肠肌间神经元的电生理作用。通过微压喷射或在培养基中施加CRH（0.2 - 20 nM）时，42个S/1型神经元中的21个以及40个AH/2型神经元中的28个出现了长时间的去极化。这些反应伴随着输入电阻增加和兴奋性增强。在CRH诱发的反应过程中，AH/2型细胞的峰后超极化受到抑制。对CRH反应的反转电位约为 - 90 mV，这与该肽导致钾通道关闭一致。在10 microM 5'-N-乙基羧酰胺腺苷（NECA，一种腺苷类似物）中孵育可阻止CRH诱导的去极化，表明该反应是由腺苷酸环化酶的刺激和cAMP升高介导的。CRH降低了快速烟碱型兴奋性突触后电位的幅度。这似乎是一种突触后作用，因为该肽也降低了对外源性乙酰胆碱的反应。这些结果表明，CRH可通过作用于肌间神经元直接影响肠道功能。
