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乙醇可降低运动神经元兴奋性,并增强人脊髓中Ia传入神经的突触前抑制。

Ethanol reduces motoneuronal excitability and increases presynaptic inhibition of Ia afferents in the human spinal cord.

作者信息

von Dincklage Falk, Benzke Michael, Rehberg Benno, Baars Jan Harald

机构信息

Charité, Universitätsmedizin Berlin, Department of Anesthesiology, Germany.

出版信息

Brain Res. 2007 Oct 10;1173:78-83. doi: 10.1016/j.brainres.2007.07.052. Epub 2007 Aug 9.

DOI:10.1016/j.brainres.2007.07.052
PMID:17825271
Abstract

INTRODUCTION

Already low blood concentrations of ethanol acutely impair motor control and coordination. In vitro experiments have given evidence that spinal effects of ethanol contribute to this by reducing spinal excitability and enhancing presynaptic inhibition of Ia fibers. In this study, we investigated the influence of 0.7 g per kilogram of bodyweight ethanol on motoneuronal excitability and presynaptic inhibition in humans.

METHODS

The study was performed in 10 volunteers. Spinal excitability was measured by the maximal H-reflex of the soleus muscle normalized to the maximal muscular response (Hmax/Mmax). Presynaptic inhibition was measured by changes in heteronymous Ia-facilitation of the soleus H-reflex, which is achieved by stimulation of the femoral nerve. A decrease in facilitation can be ascribed to an increase in presynaptic inhibition. Changes of these parameters under the influence of 0.7 g per kilogram of bodyweight ethanol were assessed in comparison to control measurements before ethanol application.

RESULTS

Both parameters, Hmax/Mmax and Heteronymous facilitation, were significantly reduced under the influence of ethanol (Wilcoxon signed-rank test with Bonferroni correction for each, p<0.01).

DISCUSSION

The increase in presynaptic inhibition by ethanol is probably caused by an increase in GABAA receptor-mediated Cl-conductance, which has been shown in spinal cord cultures. The role of presynaptic inhibition in movement is assumed to be there to control the afferent input of muscle spindles and tendon organs as a mechanism of specific input-selection. This study demonstrated that ethanol reduces spinal excitability and increases GABAergic presynaptic inhibition on Ia afferent fibers in humans.

摘要

引言

乙醇血液浓度本就较低时,会急性损害运动控制和协调能力。体外实验已证明,乙醇对脊髓的作用通过降低脊髓兴奋性和增强Ia纤维的突触前抑制来促成这一现象。在本研究中,我们调查了每千克体重0.7克乙醇对人体运动神经元兴奋性和突触前抑制的影响。

方法

该研究在10名志愿者身上进行。通过将比目鱼肌的最大H反射归一化至最大肌肉反应(Hmax/Mmax)来测量脊髓兴奋性。通过刺激股神经实现比目鱼肌H反射的异源Ia易化变化来测量突触前抑制。易化的降低可归因于突触前抑制的增加。与乙醇应用前的对照测量相比,评估了每千克体重0.7克乙醇影响下这些参数的变化。

结果

在乙醇影响下,Hmax/Mmax和异源易化这两个参数均显著降低(均采用经Bonferroni校正的Wilcoxon符号秩检验,p<0.01)。

讨论

乙醇引起的突触前抑制增加可能是由脊髓培养中已显示的GABAA受体介导的Cl电导增加所致。突触前抑制在运动中的作用被认为是控制肌梭和腱器官的传入输入,作为一种特定输入选择机制。本研究表明,乙醇会降低人体脊髓兴奋性,并增加对Ia传入纤维的GABA能突触前抑制。

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