Dynamic rewiring of neural circuits in the motor cortex in mouse models of Parkinson's disease.
Dynamic rewiring of neural circuits in the motor cortex in mouse models of Parkinson's disease.
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DOI：
10.1038/nn.4082
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发表时间：
2015-09
影响因子：
25
通讯作者：
Ding JB
中科院分区：
文献类型：
--
作者：
Guo L;Xiong H;Kim JI;Wu YW;Lalchandani RR;Cui Y;Shu Y;Xu T;Ding JB
突触可塑性的动态适应对于学习新的运动技能和维持终身记忆至关重要，而帕金森病（PD）会迅速下降。运动皮层的可塑性对于获得和维持新的运动技能是重要的，但是PD中多巴胺的丢失如何导致运动皮层的结构和功能可塑性被破坏尚不清楚。在这里，我们利用小鼠模型的PD和双光子成像表明，多巴胺耗竭导致运动皮层的结构变化。我们进一步发现，多巴胺D1和D2受体信号与选择性和明显地调节这些结构和功能可塑性的异常变化有关。我们的研究结果表明，D1和D2受体信号调节运动皮层的可塑性，多巴胺的损失导致非典型的突触适应，可能有助于在PD中观察到的运动性能和运动记忆的损害。
Dynamic adaptations in synaptic plasticity are critical for learning new motor skills and maintaining memory throughout life, which rapidly decline with Parkinson's disease (PD). Plasticity in the motor cortex is important for acquisition and maintenance of novel motor skills, but how the loss of dopamine in PD leads to disrupted structural and functional plasticity in the motor cortex is not well understood. Here, we utilized mouse models of PD and 2-photon imaging to show that dopamine depletion resulted in structural changes in the motor cortex. We further discovered that dopamine D1 and D2 receptor signaling were linked to selectively and distinctly regulating these aberrant changes in structural and functional plasticity. Our findings suggest that both D1 and D2 receptor signaling regulate motor cortex plasticity, and loss of dopamine results in atypical synaptic adaptations that may contribute to the impairment of motor performance and motor memory observed in PD.