Basal ganglia integration of postural muscle tone and locomotion.

基底神经节疾病的特征是运动量和肌张力异常。步态障碍也是帕金森病患者的主要障碍。有人认为，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，控制肌肉张力和运动是通过基底神经节脑干系统。在急性去脑猫中，纹状体、丘脑和大脑皮层被移除，一系列刺激传递到中脑运动区（MLR）产生受控运动。此外，施加到脚桥核（PPN）的刺激序列抑制姿势性肌张力。此外，神经解剖学研究表明，MLR/PPN区域接受来自黑质网状部（SNr）（基底神经节的输出核）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。 ...更多信息 肌肉张力重复的刺激单独提供给SNr诱发肌肉活动没有变化。然而，刺激SNr的内侧部分抑制MLR诱发的运动。在低强度下，SNr刺激减少了MLR激活的步周期的数量，在较高的刺激强度下，运动被取消。此外，随着SNr刺激强度的增加，MLR诱发的运动的开始被延迟。这些发现表明，SNr有助于启动和维持MLR诱导的运动。此外，PPN诱导的肌张力抑制在低强度刺激SNr的外侧部分时减弱，并在较高的刺激强度下消失。进一步观察到上述SNr效应可被MLR和PPN内注射GABAA拮抗剂所阻断。这些结果均提示运动和姿势肌张力受GABA能黑质被盖投射的调节。目前的工作表明，基底神经节疾病可能包括黑被盖系统功能障碍，随之而来的步态和肌张力障碍。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