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去大脑猫排尿过程中括约肌运动神经元的膜电位变化

Membrane potential changes in sphincter motoneurons during micturition in the decerebrate cat.

作者信息

Fedirchuk B, Shefchyk S J

机构信息

Department of Medicine, University of Manitoba, Winnipeg, Canada.

出版信息

J Neurosci. 1993 Jul;13(7):3090-4. doi: 10.1523/JNEUROSCI.13-07-03090.1993.

DOI:10.1523/JNEUROSCI.13-07-03090.1993
PMID:8331386
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6576663/
Abstract

Intracellular recordings from external urethral sphincter (EUS) and external anal sphincter (EAS) motoneurons were obtained during micturition in the decerebrate cat. The neural circuitry mediating micturition was activated by distension of the bladder or by electrical stimulation of the pontine micturition center (PMC). During micturition, the membrane potential of EUS motoneurons hyperpolarized 3-9 mV, during which time the motoneuron somatic membrane conductance increased. The membrane hyperpolarization could be reversed with passive diffusion or active ejection of chloride from the intracellular microelectrode into the motoneuron. In contrast, the membrane potential of EAS motoneurons either depolarized slightly or showed no change during micturition. We have shown that the neural circuitry mediating micturition can influence the EUS and EAS independently. In addition, stimulation of the PMC provides a valuable tool for identifying spinal neurons mediating the postsynaptic inhibition of EUS motoneurons during micturition.

摘要

在去大脑猫排尿过程中,获取了来自尿道外括约肌(EUS)和肛门外括约肌(EAS)运动神经元的细胞内记录。介导排尿的神经回路通过膀胱扩张或脑桥排尿中枢(PMC)的电刺激来激活。在排尿过程中,EUS运动神经元的膜电位超极化3 - 9 mV,在此期间运动神经元的体细胞膜电导增加。膜超极化可通过氯离子从细胞内微电极被动扩散或主动排出到运动神经元中而逆转。相比之下,EAS运动神经元的膜电位在排尿过程中要么轻微去极化,要么没有变化。我们已经表明,介导排尿的神经回路可以独立影响EUS和EAS。此外,刺激PMC为识别在排尿过程中介导EUS运动神经元突触后抑制的脊髓神经元提供了一种有价值的工具。