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猫迷走神经 cardio - 抑制性神经元吸气调制中涉及的突触机制。

Synaptic mechanisms involved in the inspiratory modulation of vagal cardio-inhibitory neurones in the cat.

作者信息

Gilbey M P, Jordan D, Richter D W, Spyer K M

出版信息

J Physiol. 1984 Nov;356:65-78. doi: 10.1113/jphysiol.1984.sp015453.

Abstract

The respiratory modulation of the activity of vagal cardio-inhibitory neurones of the nucleus ambiguus of the cat has been investigated by electrophysiological and neuropharmacological techniques. All twenty-four vagal efferent neurones studied had axons with conduction velocities indicative of B fibres and projected to the right cardiac branches of the vagus. Their spontaneous or DL-homocysteic acid (DLH)-evoked activity showed a marked reduction during the phase of inspiration and all showed signs of receiving a baroreceptor input. Ionophoretic application of DLH always excited cardiac vagal motoneurones (c.v.m.s). Application of acetylcholine to these same cells provoked a decrease in firing rate in twelve of the fifteen neurones tested. In ten of these twelve cells simultaneous application of atropine antagonized the effect of acetylcholine. Atropine applied alone enhanced neuronal firing, particularly in inspiration. Stable intracellular recordings have been made from two c.v.m.s. These were inhibited during inspiration. Input resistance fell markedly during inspiration and injection of chloride reversed this wave of hyperpolarization to a wave of depolarization indicating that this resulted from chloride-mediated inhibitory post-synaptic potentials (i.p.s.p.s). These c.v.m.s were activated during Stage I expiration, and showed a weak and variable wave of inhibition in Stage II expiration. Pulse-rhythmic depolarizing potentials were reduced in their amplitudes during the periods of decreased neurone input resistance. It is concluded that c.v.m.s receive an excitatory input during post-inspiration and a powerful inhibitory synaptic input during inspiration. The implications of these observations for the physiology of cardiorespiratory reflexes are discussed.

摘要

运用电生理学和神经药理学技术,对猫疑核迷走神经心抑制神经元活动的呼吸调制进行了研究。所研究的24个迷走神经传出神经元,其轴突传导速度均表明为B纤维,并投射至迷走神经右心支。它们的自发活动或由DL-高胱氨酸(DLH)诱发的活动,在吸气阶段显著降低,且均显示出接受压力感受器输入的迹象。离子电泳施加DLH总能兴奋心脏迷走运动神经元(c.v.m.s)。对这些相同的细胞施加乙酰胆碱,在测试的15个神经元中有12个神经元的放电频率降低。在这12个细胞中的10个细胞中,同时施加阿托品可拮抗乙酰胆碱的作用。单独施加阿托品可增强神经元放电,尤其是在吸气时。已从两个c.v.m.s进行了稳定的细胞内记录。这些在吸气时受到抑制。吸气期间输入电阻显著下降,注入氯化物可使这种超极化波反转成去极化波,表明这是由氯化物介导的抑制性突触后电位(i.p.s.p.s)所致。这些c.v.m.s在I期呼气时被激活,在II期呼气时表现出微弱且多变的抑制波。在神经元输入电阻降低期间,脉冲节律性去极化电位的幅度减小。得出的结论是,c.v.m.s在吸气后接受兴奋性输入,在吸气时接受强大的抑制性突触输入。讨论了这些观察结果对心肺反射生理学的意义。

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