Mechanisms of use-dependent plasticity in the human motor cortex.
Mechanisms of use-dependent plasticity in the human motor cortex.
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DOI：
10.1073/pnas.97.7.3661
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发表时间：
2000-03
影响因子：
11.1
通讯作者：
C. Bütefisch;B. Davis;Steven P. Wise;L. Sawaki;L. Kopylev;Joseph Classen;Leonardo G. Cohen
中科院分区：
文献类型：
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作者：
C. Bütefisch;B. Davis;Steven P. Wise;L. Sawaki;L. Kopylev;Joseph Classen;Leonardo G. Cohen
练习动作可以提高运动能力和运动皮层的可塑性。为了确定潜在的机制，我们研究了人类受试者的使用依赖性可塑性，这些受试者预先服用了影响突触可塑性的药物。美沙芬（一种N-甲基-d-天冬氨酸受体阻滞剂）和劳拉西泮（一种γ-氨基丁酸（GABA）A型受体阳性变构调节剂）显著降低了多巴胺依赖性可塑性。这些结果确定N-甲基-d-天冬氨酸受体激活和GABA能抑制作为在完整的人类运动皮层中使用依赖性可塑性中起作用的机制，并指出这种形式的可塑性和长时程增强的机制的相似性。
Practicing movements results in improvement in performance and in plasticity of the motor cortex. To identify the underlying mechanisms, we studied use-dependent plasticity in human subjects premedicated with drugs that influence synaptic plasticity. Use-dependent plasticity was reduced substantially by dextromethorphan (an N-methyl-d-aspartate receptor blocker) and by lorazepam [a gamma-aminobutyric acid (GABA) type A receptor-positive allosteric modulator]. These results identify N-methyl-d-aspartate receptor activation and GABAergic inhibition as mechanisms operating in use-dependent plasticity in intact human motor cortex and point to similarities in the mechanisms underlying this form of plasticity and long-term potentiation.