生物谷報道：今天（1月14日）剛剛出版的Cell正式刊出中國科學院神經科學研究所的文章,，早在兩個月前，生物谷首次公開報道,，Cell正式接收中國大陸近二十五年來第一篇原創(chuàng)性Cell文章,，是中國生命科學領域的重大的突破，詳細見：中科院神經所蔣輝博士的論文已被Cell接收,，生物谷報道后,，在國內引起了極大的反響，被全國各大網站,，BBS轉載,，同時許多研究工作者發(fā)表了精彩的評論，如管中窺豹——從蔣輝的信看神經所氛圍,，為促進國內生命科學的發(fā)展起到積極的推動作用,。
蔣輝博士在這篇報道中發(fā)現(xiàn)：GSK蛋白質的活性對確定神經細胞極性起關鍵作用，開拓了治療神經損傷的新途徑,。
這篇具有開創(chuàng)性意義的文章主要來自于中科院上海生命科學研究院神經科學研究所，也是神經所近數年來發(fā)表的一系列重大文章之一,，附后（文章均可下載）,。
腦神經復雜的信息傳導有賴神經細胞的特殊結構，神經細胞通常有兩種結構 接收訊號的樹突,、發(fā)送訊號的軸突,。他們的研究揭示了神經細胞的這兩個基本極性是如何形成的，GSK蛋白激酶在發(fā)育過程中的分布有極性,，在軸突中的活性比樹突中要低,。如果其活性太高，神經細胞會沒有軸突,，太低則會把樹突變成軸突,。它的活性由上游分子來調控，多個分子形成通路,，控制著神經細胞的極性,。還發(fā)現(xiàn)，確定神經細胞極性的GSK還維持著極性,。如果用藥物改變GSK活性,，就可以把樹突變成軸突。這表明,，可以通過藥物來增加軸突數量,，這可能成為神經元損傷修復和退行性神經系統(tǒng)疾病治療的新突破口。
Axon-dendrite polarity is a cardinal feature of neuronal morphology essential for information flow. Here we report a differential distribution of GSK-3 activity in the axon versus the dendrites. A constitutively active GSK-3 mutant inhibited axon formation, whereas multiple axons formed from a single neuron when GSK-3 activity was reduced by pharmacological inhibitors, a peptide inhibitor, or siRNAs. An active mechanism for maintaining neuronal polarity was revealed by the conversion of preexisting dendrites into axons upon GSK-3 inhibition. Biochemical and functional data show that the Akt kinase and the PTEN phosphatase are upstream of GSK-3 in determining neuronal polarity. Our results demonstrate that there are active mechanisms for maintaining as well as establishing neuronal polarity, indicate that GSK-3 relays signaling from Akt and PTEN to play critical roles in neuronal polarity, and suggest that application of GSK-3 inhibitors can be a novel approach to promote generation of new axons after neural injuries.
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相關報道：
管中窺豹——從蔣輝的信看神經所氛圍
中科院神經所蔣輝博士的論文已被Cell接收
饒毅博士簡介
蒲慕明所長在神經所2003年所年會上的講話
蒲慕明教授對神經所的新年祝詞
蒲慕明博士簡介 href="http://www.bioon.com/biology/talent/chinese/200411/83869.html" target=_blank>蒲慕明博士簡介
附1：
神經所近三年內已發(fā)表的重要文章[PDF文件全部可以下載]
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