近日，日本一個研究小組在最新一期英國雜志《腦》Brain上發(fā)表文章說,，一側肢體不能正?；顒拥膶嶒炇螅浯竽X未受損一側的神經(jīng)會“補缺”,，部分接替受損一側大腦神經(jīng)的功能,。
日本大阪大學教授山下俊英領導的研究小組說，從左右腦延伸出的神經(jīng)在腦的延髓處交叉,，右腦負責左半身,，左腦負責右半身。腦的一側出現(xiàn)腦血管障礙或腦挫傷等損傷時,，相反一側的手腳就會出現(xiàn)麻痹甚至半身不遂,。
研究小組人為損傷了實驗鼠左腦，結果實驗鼠右前腳麻痹,，不能正?；顒樱s4周后，實驗鼠的運動功能恢復到了原有水平的一半左右,。研究小組發(fā)現(xiàn),，實驗鼠右腦中控制左前腳運動的神經(jīng)細胞的神經(jīng)突觸向左腦中控制右前腳運動的神經(jīng)細胞伸展，并與其連接,。
研究小組還發(fā)現(xiàn),，神經(jīng)細胞分泌的一種神經(jīng)營養(yǎng)因子“BDNF”能促進這些神經(jīng)突觸的伸展，人為抑制這種蛋白質(zhì)作用,，小鼠的受損一側肢體運動機能恢復就會變得困難和緩慢,。研究人員認為，通過康復運動能刺激這種蛋白質(zhì)的分泌,。（生物谷Bioon.com）
doi:10.1093/brain/aws053
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Intraspinal rewiring of the corticospinal tract requires target-derived brain-derived neurotrophic factor and compensates lost function after brain injury
Masaki Ueno1,2, Yasufumi Hayano1,2, Hiroshi Nakagawa1,2 and Toshihide Yamashita1,2
Brain injury that results in an initial behavioural deficit is frequently followed by spontaneous recovery. The intrinsic mechanism of this functional recovery has never been fully understood. Here, we show that reorganization of the corticospinal tract induced by target-derived brain-derived neurotrophic factor is crucial for spontaneous recovery of motor function following brain injury. After destruction of unilateral sensorimotor cortex, intact-side corticospinal tract formed sprouting fibres into the specific lamina of the denervated side of the cervical spinal cord, and made new contact with two types of spinal interneurons—segmental and propriospinal neurons. Anatomical and electrophysiological analyses revealed that this rewired corticospinal tract functionally linked to motor neurons and forelimb muscles. This newly formed corticospinal circuit was necessary for motor recovery, because transection of the circuit led to impairment of recovering forelimb function. Knockdown of brain-derived neurotrophic factor in the spinal neurons or its receptor in the intact corticospinal neurons diminished fibre sprouting of the corticospinal tract. Our findings establish the anatomical, functional and molecular basis for the intrinsic capacity of neurons to form compensatory neural network following injury.
