Schneider Cyril, Devanne Hervé, Lavoie Brigitte A, Capaday Charles
Department of Anatomy and Physiology, Centre de Recherche Université Laval-Robert Giffard, Quebec G1J 2G3, Canada.
Exp Brain Res. 2002 Sep;146(1):86-94. doi: 10.1007/s00221-002-1137-2. Epub 2002 Jul 23.
We sought to understand the basic neural processes involved in the functional linking of motor cortical points. We asked which of the two basic neural mechanisms, excitation or inhibition, is required to functionally link motor cortical points. In the ketamine-anaesthetized cat, a microstimulation electrode was positioned at a point (control point) that was identified by the following three characteristics of the EMG responses: the muscle(s) activated at threshold, any additional muscles recruited by supra-threshold stimulation, and their relative latency. A second distinct point (test point) producing activation of a muscle at a different joint was then identified. At this test cortical point the GABA(A) receptor antagonist bicuculline was ejected iontophoretically, while stimulating the control point near threshold. A combined response was elicited consisting of the response normally elicited at the control point plus that elicited at the test point. Thus, an artificial muscle synergy was produced following disinhibition of the test point. This was never the case when glutamate was ejected at the test point, even when supra-threshold stimuli were used at the control point. Therefore, simply increasing the excitability of a cortical point was not sufficient to release the muscle(s) represented at that point into a muscle synergy. Kynurenate, a broadly acting excitatory amino acid receptor antagonist, ejected at the bicuculline point reversed the effect of bicuculline. This shows that the release phenomenon was mediated synaptically and was not due to spread of the stimulating current. We suggest that release from inhibition may be one of the neural mechanisms involved in functionally linking motor cortical points. This functional linking may be part of the ensemble of motor cortical mechanisms involved in recruitment of muscle synergies.
我们试图了解运动皮层各点功能连接所涉及的基本神经过程。我们探究在功能连接运动皮层各点时，两种基本神经机制（兴奋或抑制）中哪一种是必需的。在氯胺酮麻醉的猫身上，将一个微刺激电极置于一个点（控制点），该点通过肌电图反应的以下三个特征来确定：阈值时激活的肌肉、阈上刺激额外募集的任何肌肉及其相对潜伏期。然后确定另一个能激活不同关节处肌肉的不同点（测试点）。在这个测试皮层点，通过离子电泳法注入GABA(A)受体拮抗剂荷包牡丹碱，同时在阈值附近刺激控制点。引发了一个复合反应，包括通常在控制点引发的反应加上在测试点引发的反应。因此，在测试点去抑制后产生了一种人工肌肉协同作用。当在测试点注入谷氨酸时，即使在控制点使用阈上刺激，情况也并非如此。因此，仅仅增加皮层点的兴奋性不足以使该点所代表的肌肉释放到肌肉协同作用中。在荷包牡丹碱作用点注入泛作用兴奋性氨基酸受体拮抗剂犬尿氨酸可逆转荷包牡丹碱的作用。这表明释放现象是通过突触介导的，并非由于刺激电流的扩散。我们认为抑制解除可能是运动皮层各点功能连接所涉及的神经机制之一。这种功能连接可能是参与募集肌肉协同作用的运动皮层机制整体的一部分。
