我们临床上发现，臂丛损伤导致大脑皮层发生动态影像学改变，提示发生了功能重塑，但目前没有臂丛损伤本身所致运动皮层动态重塑机制的报道。鉴于已有研究显示MHCI、PirB、CD3ζ蛋白可调控视觉皮层重塑，因此假设，在臂丛损伤早期，去传入冲动在抑制臂丛皮层代表区和增加其周围兴奋性同时，也使周围皮层上述3个蛋白活性增加，这在一定程度上抑制了周围皮层对臂丛代表区的"侵占"。但随着躯干和肩部等代偿性动作增加，功能活跃的周围皮层与臂丛代表区仍逐渐形成新的神经连接网络，从而使前者区域内上述蛋白回到基线水平。将在皮层重塑的大鼠模型上，用qPCR和Western Blot定量检测上述蛋白的表达量，用原位杂交和免疫荧光染色定位脑组织切片中目标蛋白变化区域所处位置。如果能在分子层面上得到与电刺激相对应的检测结果，就有理由确认临床有影像学改变的臂丛代表区域发生了功能重塑，这将为制定抑制有害重塑的康复措施提供理论依据。

Clinically, we found by resting-state fMRI test that brachial plexus injuries induced dynamic imaging changes in representations of the brachial plexus of brain cortex, which suggested functional re-organization in that area. Till now, however, no study has been reported of the machnism of the dynamic plasticity in the motor cortex caused by brachial plexus injuries per se. As some studies have showed that MHCI, PirB and CD3 zeta proteins can regulate the plasticity of visual cortex, we hypothesize that during the early stage of brachial plexus injuries,the deafferentation can make representations of the brachial plexus in the brain cortex inhibited, so that the neural excitbility is enhanced of the adjacent non-deafferented cortices; MHCI, PirB and CD3 zeta proteins in these adjacent areas, therefore, are also functionally activated to a higher level for the purpose of preventing "take-over" of surrounding cortices to representations of the brachial plexus. But as compensatory actions of the torso and shoulder increase, new neural network is still gradually established between representations of the brachial plexus and adjacent non-deafferented cortices, so that the expression level of three proteins metioned above returns to baseline. After constructiion of the rat model simulating functional re- organization of the motor cortex of the brachial plexus, qPCR and Western Blot are used to quantify the expression level of the target proteins, and in situ hybridization and immunofluorescence staining are applied to locate the changing areas of the these proteins in brain tissue slices. If molecular and electrical stimulating results were well matched in the rat model, it is reasonable to believe that clinical dynamic imaging changes in cortical representations of the brachial plexus after brachial plexopathy, mean the occurranve of neural plasticity in these areas. This will provide theoretical basis for application of rehabilitation measures to inhibit this "harmful" plasticity.