Oscillatory circuits underlying locomotor networks in the rat spinal cord.

Giuliano Taccola, Andrea Nistri
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引用次数: 20

Abstract

The mammalian thoracolumbar spinal cord contains all the necessary elements to generate a rhythmic oscillatory activity that is transformed into locomotor commands to agonist and antagonist limb muscles to produce gait at various speed. This motor program is produced by interneurons in the ventral horn and can be readily recorded even with in vitro spinal cord preparations isolated from rats or mice (once dorsal afferents are stimulated or excitatory neuronchemicals applied). The locomotor program is continuously modulated and refined by afferent sensory inputs and by signals descending from brain centers. Nevertheless, this program is not the only type of rhythmic discharge produced by spinal networks. In fact, activation of metabotropic group I glutamate receptors or block of certain K+ currents by 4-aminopyridine generates non-locomotor discharges, and, at the same time, facilitates evoked locomotor activity, which then suppresses any other interfering rhythmicity. These findings suggest that accessory networks, activated by suitable stimuli, might be exploited to restore locomotor activity damaged by a lesion, an obvious goal for neuro-rehabilitation purposes. The structure of the locomotor networks appears to include a rhythm-generating circuit that drives a pattern formation circuit, commanding motoneurons to discharge appropriate signals to skeletal muscles. Studies with the K+-channel blocker tetraethylammonium have indicated that this hierarchical arrangement is preserved in vitro. Hence, isolated spinal cord preparations represent an interesting experimental tool to investigate new mechanisms to upregulate various components of locomotor networks, especially after the induction of experimental lesions.

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大鼠脊髓运动网络下的振荡回路。
哺乳动物胸腰段脊髓包含产生节律性振荡活动的所有必要元素,该活动转化为运动命令,以激动剂和拮抗剂肢体肌肉产生不同速度的步态。这种运动程序是由腹侧角的中间神经元产生的,即使从大鼠或小鼠身上分离出体外脊髓制剂(一旦刺激背侧传入事件或应用兴奋性神经化学物质),也可以很容易地记录下来。运动程序由传入的感觉输入和来自大脑中心的信号不断调节和完善。然而,这个程序并不是脊椎网络产生的唯一一种有节奏的放电。事实上,4-氨基吡啶激活代谢I组谷氨酸受体或阻断某些K+电流会产生非运动放电,同时促进诱发的运动活动,从而抑制任何其他干扰性节律。这些发现表明,在适当的刺激下激活的副神经网络可能被用来恢复被损伤的运动活动,这是神经康复的一个明显目标。运动网络的结构似乎包括一个产生节奏的回路,它驱动模式形成回路,命令运动神经元向骨骼肌发出适当的信号。用K+通道阻滞剂四乙基铵进行的研究表明,这种分层排列在体外是保留的。因此,孤立脊髓制剂是一种有趣的实验工具,可以研究上调运动网络各种成分的新机制,特别是在实验性病变诱导后。
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