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(cè)肢體不能正常活動的實驗鼠,，其大腦未受損一側(cè)的神經(jīng)會“補缺”,，部分接替受損一側(cè)大腦神經(jīng)的功能。
日本大阪大學(xué)教授山下俊英領(lǐng)導(dǎo)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(fù)責(zé)左半身，左腦負(fù)責(zé)右半身,。腦的一側(cè)出現(xiàn)腦血管障礙或腦挫傷等損傷時,，相反一側(cè)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(jié)果實驗鼠右前腳麻痹,，不能正常活動,，但約4周后,，實驗鼠的運動功能恢復(fù)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(xì)胞的神經(jīng)突觸向左腦中控制右前腳運動的神經(jīng)細(xì)胞伸展,，并與其連接。
研究小組還發(fā)現(xiàn)，神經(jīng)細(xì)胞分泌的一種神經(jīng)營養(yǎng)因子“BDNF”能促進(jìn)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(cè)肢體運動機能恢復(fù)就會變得困難和緩慢。研究人員認(rèn)為,，通過康復(fù)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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PMID:
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.
