Ethier Christian, Brizzi Laurent, Giguère Dominic, Capaday Charles
CRULRG Brain and Movement Laboratory, Department of Anatomy and Physiology, Faculty of Medicine, Laval University, F-6500, 2601 de la Canardière, Québec City (QC), Canada G1J 2G3.
Eur J Neurosci. 2007 Sep;26(6):1632-41. doi: 10.1111/j.1460-9568.2007.05778.x.
We recently suggested that movement-related inter-joint muscle synergies are recruited by selected excitation and selected release from inhibition of cortical points. Here we asked whether a similar cortical mechanism operates in the functional linking of antagonistic muscles. To this end experiments were done on ketamine-anesthetized cats. Intracortical microstimulation (ICMS) and intramuscular electromyographic recordings were used to find and characterize wrist, elbow and shoulder antagonistic motor cortical points. Simultaneous ICMS applied at two cortical points, each evoking activity in one of a pair of antagonistic muscles, produced co-contraction of antagonistic muscle pairs. However, we found an obvious asymmetry in the strength of reciprocal inhibition; it was always significantly stronger on physiological extensors than flexors. Following intravenous injection of a single bolus of strychnine, a cortical point at which only a physiological flexor was previously activated also elicited simultaneous activation of its antagonist. This demonstrates that antagonistic corticospinal neurons are closely grouped, or intermingled. To test whether releasing a cortical point from inhibition allows it to be functionally linked with an antagonistic cortical point, one of three GABA(A) receptor antagonists, bicuculline, gabazine or picrotoxin, was injected iontophoretically at one cortical point while stimulation was applied to an antagonistic cortical point. This coupling always resulted in co-contraction of the represented antagonistic muscles. Thus, antagonistic motor cortical points are linked by excitatory intracortical connections held in check by local GABAergic inhibition, with reciprocal inhibition occurring at the spinal level. Importantly, the asymmetry of cortically mediated reciprocal inhibition would appear significantly to bias muscle maps obtained by ICMS in favor of physiological flexors.
我们最近提出，与运动相关的关节间肌肉协同作用是通过对皮质点的选择性兴奋和抑制释放来招募的。在这里，我们研究了类似的皮质机制是否在拮抗肌的功能连接中起作用。为此，我们对氯胺酮麻醉的猫进行了实验。采用皮质内微刺激（ICMS）和肌内肌电图记录来寻找和表征腕部、肘部和肩部的拮抗运动皮质点。在两个皮质点同时施加ICMS，每个点在一对拮抗肌中的一块肌肉中诱发活动，结果产生了拮抗肌对的共同收缩。然而，我们发现交互抑制的强度存在明显的不对称性；生理伸肌上的交互抑制总是明显强于屈肌。静脉注射单次大剂量的士的宁后，一个之前仅能激活生理屈肌的皮质点也能诱发其拮抗肌的同时激活。这表明拮抗的皮质脊髓神经元紧密聚集或相互交织。为了测试从抑制中释放一个皮质点是否能使其与拮抗皮质点建立功能连接，在一个皮质点离子导入注射三种GABA(A)受体拮抗剂之一（荷包牡丹碱、加巴喷丁或印防己毒素），同时刺激拮抗皮质点。这种耦合总是导致所代表的拮抗肌共同收缩。因此，拮抗运动皮质点通过局部GABA能抑制控制的兴奋性皮质内连接相连，交互抑制发生在脊髓水平。重要的是，皮质介导的交互抑制的不对称性似乎会显著偏向通过ICMS获得的肌肉图谱，有利于生理屈肌。
