Tests for presynaptic modulation of corticospinal terminals from peripheral afferents and pyramidal tract in the macaque
Tests for presynaptic modulation of corticospinal terminals from peripheral afferents and pyramidal tract in the macaque
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DOI：
10.1113/jphysiol.2005.100537
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发表时间：
2006-05-15
影响因子：
5.5
通讯作者：
Fetz, E. E.
中科院分区：
文献类型：
--
作者：
Jackson, A.;Baker, S. N.;Fetz, E. E.
脊髓感觉输入的有效性可以在随意运动期间通过使传入终端去极化和减少递质释放的机制在突触前调节。目前尚不清楚是否类似的影响施加在旧大陆灵长类动物和人类皮质脊髓通路的下行纤维末端。我们研究了猕猴上臂周围神经（正中、桡侧和尺侧）和锥体束刺激后皮质脊髓通路突触前抑制的两个特征：(1)皮质脊髓轴突终端的兴奋性增加，这是由皮质反生理诱发电位的变化所揭示的；(2)脊髓皮质脊髓单突触场电位的大小变化。锥体束的条件反射刺激在相同的时间内增加了终末兴奋性和单突触场。兴奋性在刺激后7.5 ~ 10 ms达到最大值，并在40 ms内恢复到基线。周围神经的调节刺激在两种测量中均无统计学意义。我们得出的结论是，外周传入不会对皮质-脊髓通路施加突触前影响，并且下行截击可能产生与增强的递质释放相关的自生性终端去极化。通过下行通路对传入终端的突触前抑制，以及外周输入对皮质脊髓效能的相互影响的缺失，将有助于在中枢启动的运动中保持运动命令的保真度。
The efficacy of sensory input to the spinal cord can be modulated presynaptically during voluntary movement by mechanisms that depolarize afferent terminals and reduce transmitter release. It remains unclear whether similar influences are exerted on the terminals of descending fibres in the corticospinal pathway of Old World primates and man. We investigated two signatures of presynaptic inhibition of the macaque corticospinal pathway following stimulation of the peripheral nerves of the arm (median, radial and ulnar) and the pyramidal tract: (1) increased excitability of corticospinal axon terminals as revealed by changes in antidromically evoked cortical potentials, and (2) changes in the size of the corticospinal monosynaptic field potential in the spinal cord. Conditioning stimulation of the pyramidal tract increased both the terminal excitability and monosynaptic fields with similar time courses. Excitability was maximal between 7.5 and 10 ms following stimulation and returned to baseline within 40 ms. Conditioning stimulation of peripheral nerves produced no statistically significant effect in either measure. We conclude that peripheral afferents do not exert a presynaptic influence on the corticospinal pathway, and that descending volleys may produce autogenic terminal depolarization that is correlated with enhanced transmitter release. Presynaptic inhibition of afferent terminals by descending pathways and the absence of a reciprocal influence of peripheral input on corticospinal efficacy would help to preserve the fidelity of motor commands during centrally initiated movement.