Basal ganglia integration of postural muscle tone and locomotion.

基底神经节紊乱的特点是运动量和肌肉张力异常。步态障碍也是帕金森患者的主要障碍。有研究认为，基底神经节通过丘脑皮质控制运动量。然而，在这里，我们提供的证据表明，肌肉张力和运动的控制是通过基底神经节-脑干系统实现的。在急性失忆猫中，去除纹状体、丘脑和大脑皮层后，传递到中脑运动区（MLR）的刺激序列产生了受控运动。此外，施加于桥脚核（PPN）的一系列刺激可抑制体位性肌张力。此外，神经解剖学研究表明，MLR/PPN区域接受基底神经节输出核黑质网状部（SNr）的gaba能投射。因此，我们通过在MLR/ ppn控制的运动和姿势中激活该系统来测试该系统的功能。仅对SNr进行重复刺激不会引起肌肉活动的变化。然而，刺激信噪比的内侧部分抑制mlr诱发的运动。在低强度下，信噪比刺激减少了mlr激活的阶跃循环次数，在高强度刺激下，运动被消除。同时，随着信噪比刺激强度的增加，mlr诱发的运动发生延迟。这些发现表明，信噪比对mlr诱导的运动的开始和维持都有贡献。此外，ppn诱导的肌张力抑制在低强度的侧信噪比刺激下减弱，在高强度刺激下消失。我们进一步观察到，在MLR和PPN中注射GABAA拮抗剂可以阻断上述SNr效应。这些结果都表明运动和体位肌张力受到gaba能黑质投射的调节。目前的工作表明，基底神经节疾病可能包括黑质系统功能障碍，随之而来的步态和肌肉张力紊乱。少

Basal ganglia disorders are characterized by the presence of abnormalities in the amount of movement and muscular tone. Gait disturbances are also major impediments for parkinsonian patients. It has been suggested that the basal ganglia control the amount of movement via thalamocortical. However, here, we provide evidence that control of muscle tone and locomotion is achieved via basal ganglia-brainstem systems. In the acute decerebrate cat, with the striatum, thalamus and cerebral cortex removed, trains of stimuli delivered to the mesencephalic locomotor region (MLR) produce controlled locomotion. In addition, trains of stimuli applied to the pedunculopontine nucleus (PPN) suppress postural muscle tone. Also, neuroanatomical studies have shown that MLR/PPN areas receive a GABAergic projection from substantia nigra pars reticulata (SNr), an output nucleus of the basal ganglia. Accordingly, we tested this system's function by activating it during MLR/PPN-controlled locomotion and postur … More al muscle tone. Repetitive stimuli delivered to SNr alone evoked no change in muscular activity. However, stimulation of the medial part of SNr suppressed MLR-evoked locomotion. At low strength, SNr stimulation reduced the number of MLR-activated step cycles and at higher stimulus strength, locomotion was abolished. Also, the onset of MLR-evoked locomotion was delayed as the strength of SNr stimulation was increased. These findings indicate that SNr contributes to both the initiation and the maintenance of MLR-induced locomotion. In addition, PPN-induced muscle tone suppression was attenuated at low-strength stimulation of the lateral portion of SNr, and abolished at higher stimulus strength. We further observed that the above SNr effects were blocked by injecting GABAA antagonists, into the MLR and PPN.These results all suggest that locomotion and postural muscle tone are subject to modulation by GABAergic nigrotegmental projections. The present work suggests that basal ganglia diseases may include dysfunction of nigrotegmental systems, with consequent disorders of gait and muscle tone. Less