Crone C
Neurophysiological Institute, University of Copenhagen.
Dan Med Bull. 1993 Nov;40(5):571-81.
Reciprocal inhibition is the automatic antagonist alpha motor neurone inhibition which is evoked by contraction of the agonist muscle. This so-called natural reciprocal inhibition is a ubiquitous and pronounced phenomenon in man and must be suspected of playing a major role in the control of voluntary movements. The spinal pathways underlying this inhibitory phenomenon were studied. The disynaptic reciprocal Ia inhibitory pathway between the tibial anterior muscle and the soleus alpha motor neurones was identified and described in man. It was shown that the inhibition can be evoked in most healthy subjects at rest, but the degree of inhibition varies considerably from one subject to another. It was concluded that it corresponds to the disynaptic reciprocal Ia inhibitory pathway which has been extensively described in animal experiments. The disynaptic reciprocal inhibition was shown to increase during the dynamic phase of a dorsiflexion movement of the foot, but not during the tonic phase. However, when the peripheral afferent feedback from the contracting muscle was blocked by ischaemia, an increase of the inhibition was revealed also during the tonic phase of the dorsiflexion. The concealment of this increase during unrestrained peripheral feedback from the muscle was thought to be due to the post-activation depression mechanism; a mechanism which was described further and which probably involves reduced transmitter release at Ia afferent terminals as a result of previous activation of these afferent fibers. Hence the hypothesis was supported that alpha motor neurones and the corresponding inhibitory interneurones, which project reciprocal inhibition to the antagonist motor neurones, are activated in parallel during voluntary contraction of agonist muscles. An additional reciprocal inhibitory mechanism, the long latency reciprocal inhibition, was described between the tibial anterior muscle and the soleus alpha motor neurones. It was shown to be evoked by group I afferent activity and it was seen at a conditioning-test interval of 3-6 msec. It was initiated by supraspinal pathways and it was seen only during dorsiflexion of the foot. The pathway underlying this inhibitory mechanism is unknown, but it was suggested that it was mediated by a propriospinal pathway. The possible contribution to reciprocal inhibition of presynaptic inhibition of soleus Ia afferent fibers was studied by an indirect method. It was concluded that this presynaptic inhibition was increased during even slight dorsiflexion of the foot and that the increase was mainly dependent upon the peripheral afferent input from the contracting muscle.(ABSTRACT TRUNCATED AT 400 WORDS)
交互抑制是由主动肌收缩所诱发的拮抗肌α运动神经元的自动抑制。这种所谓的自然交互抑制在人类中是一种普遍且显著的现象，必定在随意运动的控制中发挥着重要作用。对这种抑制现象背后的脊髓通路进行了研究。在人类中识别并描述了胫骨前肌与比目鱼肌α运动神经元之间的双突触交互Ia抑制通路。结果表明，在大多数健康受试者休息时即可诱发这种抑制，但不同受试者之间的抑制程度差异很大。得出的结论是，它与在动物实验中已被广泛描述的双突触交互Ia抑制通路相对应。双突触交互抑制在足部背屈运动的动态阶段增加，但在紧张性阶段不增加。然而，当收缩肌肉的外周传入反馈因缺血而被阻断时，在背屈的紧张性阶段也会出现抑制增加。在肌肉不受限制的外周反馈期间这种增加被掩盖，被认为是由于激活后抑制机制；这是一种被进一步描述的机制，可能涉及由于这些传入纤维先前的激活导致Ia传入终末递质释放减少。因此，该假设得到了支持，即在主动肌随意收缩期间，α运动神经元以及向拮抗肌运动神经元投射交互抑制的相应抑制性中间神经元会同时被激活。在胫骨前肌与比目鱼肌α运动神经元之间描述了另一种交互抑制机制，即长潜伏期交互抑制。它由I类传入活动诱发，在3 - 6毫秒的条件 - 测试间隔时出现。它由脊髓上通路启动，仅在足部背屈时出现。这种抑制机制背后的通路尚不清楚，但有人认为它是由脊髓 propriospinal 通路介导的。通过间接方法研究了比目鱼肌Ia传入纤维的突触前抑制对交互抑制的可能贡献。得出的结论是，在足部即使轻微背屈时这种突触前抑制也会增加，且这种增加主要依赖于收缩肌肉的外周传入输入。（摘要截取自400字）
