THE MODIFICATION OF LUMBAR MOTONEURONE EXCITABILITY BY STIMULATION OF A PUTATIVE 5‐HYDROXYTRYPTAMINE PATHWAY

THE MODIFICATION OF LUMBAR MOTONEURONE EXCITABILITY BY STIMULATION OF A PUTATIVE 5‐HYDROXYTRYPTAMINE PATHWAY
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通过刺激推定的 5-羟色胺途径来改变腰椎运动神经元兴奋性

DOI:
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发表时间:
1974
影响因子:
7.3
通讯作者:
M. Roberts
M. Roberts
中科院分区:
医学2区
文献类型:
--
作者:
S. Barasi;M. Roberts

文献摘要

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1通过记录氟烷麻醉大鼠前根的脊髓反射活动来监测腰椎运动神经元兴奋性的变化。2电刺激中缝正中核可通过一条传导速度较慢的通路增加单突触反射的幅度。刺激脑干下部的其他部位效果较差。运动神经元兴奋性的这种增加通过静脉注射l-色氨酸而增强,并通过静脉注射麦角酰二乙胺(LSD)、麦角新碱或西那色林而降低。3用6个微电泳电极记录刺激背根或腹根的细胞外场电位反应。刺激中缝正中核和离子电渗应用5-羟色胺(5-HT)都增加了腰椎运动神经元的兴奋性,表现为场电位振幅的增加。4电离子导入Cinanserin和methysergide可降低刺激中缝核和电离子导入5-HT的反应。5讨论了腰运动神经元对5-HT的反应和中缝-脊髓通路内活动的相似性。研究表明,中缝脊髓通路内的活动可以通过脊髓前角释放5-HT来增加腰运动神经元的兴奋性。
1 Changes in lumbar motoneurone excitability were monitored by recording spinal reflex activity from the ventral roots of rats anaesthetized with fluothane. 2 Electrical stimulation of nucleus raphes medianus increased the amplitude of the monosynaptic reflex via a pathway having a slow conduction velocity. Stimulation elsewhere in the lower brain stem was less effective. This increase in motoneurone excitability was potentiated by the intravenous injection of l‐tryptophan and reduced by intravenous injections of lysergic acid diethylamide (LSD), methysergide or Cinanserin. 3 Extracellular field potential responses to stimulation of dorsal or ventral roots were recorded with six barrelled microiontophoresis electrodes. Stimulation of nucleus raphes medianus and iontophoretic application of 5‐hydroxytryptamine (5‐HT) both increased the excitability of lumbar motoneurones as reflected by an increase in field potential amplitude. 4 Responses to both stimulation of raphe nuclei and iontophoretic application of 5‐HT were reduced by iontophoretic application of Cinanserin and methysergide. 5 The similarities of the responses of lumbar motoneurones to applied 5‐HT and activity within the raphe‐spinal pathway are discussed. It is suggested that activity within the raphe‐spinal pathway can increase lumbar motoneurone excitability via the release of 5‐HT in the ventral horn of the spinal cord.