2009年7月13日國際雜志《細(xì)胞生物學(xué)期刊》（Journal of Cell Biology）發(fā)表了中國科學(xué)院上海生命科學(xué)研究院神經(jīng)科學(xué)研究所段樹民實(shí)驗(yàn)室童小萍等的研究論文“GABA通過激活鈉通道和鈉-鈣交換通路而引起的鈣信號對NG2膠質(zhì)細(xì)胞遷移的作用”。同期雜志在“本期新聞”欄目以題為“腦修復(fù)細(xì)胞對GABA的跟隨反應(yīng)”的短文對該論文給予重點(diǎn)介紹,。
NG2膠質(zhì)細(xì)胞又被稱為少突膠質(zhì)前體細(xì)胞,，在腦發(fā)育早期產(chǎn)生少突膠質(zhì)細(xì)胞以形成中樞神經(jīng)的髓鞘。在成熟腦內(nèi)也有大量的NG2細(xì)胞, 可能對腦損傷后的髓鞘修復(fù)起重要作用,。NG2膠質(zhì)細(xì)胞的一個重要特征是象神經(jīng)元一樣表達(dá)鈉通道,，但這些鈉通道卻不能產(chǎn)生神經(jīng)元那樣的動作電位，因此NG2膠質(zhì)細(xì)胞所表達(dá)的鈉通道的功能一直不清楚,。童小萍等應(yīng)用多種手段研究表明NG2膠質(zhì)細(xì)胞表達(dá)的鈉通道有一種慢失活成份,。進(jìn)一步研究發(fā)現(xiàn)NG2膠質(zhì)細(xì)胞對神經(jīng)遞質(zhì)GABA的反應(yīng)和非成熟神經(jīng)元的反應(yīng)一樣，都是產(chǎn)生興奮性去極化反應(yīng),，并使細(xì)胞內(nèi)鈣升高,。與非成熟神經(jīng)元的反應(yīng)不同的是，GABA引起的NG2細(xì)胞鈣升高并不是通過鈣通道的激活,，而是由于激活了鈉通道的慢失活成份,，從而使細(xì)胞內(nèi)鈉升高，繼而通過鈉-鈣交換體使細(xì)胞內(nèi)鈣升高,。進(jìn)一步研究表明這一新穎的鈣升高通路對GABA引起的NG2膠質(zhì)細(xì)胞在腦內(nèi)的遷移起關(guān)鍵作用,。這些發(fā)現(xiàn)不但揭示了NG2膠質(zhì)細(xì)胞新穎的鈣信號機(jī)制,，對理解發(fā)育早期NG2細(xì)胞在腦內(nèi)的遷移機(jī)理及腦損傷后NG2細(xì)胞向損傷區(qū)遷移并參與髓鞘修復(fù)的機(jī)理也具有重要意義。（生物谷Bioon.com）
生物谷推薦原始出處：
The Journal of Cell Biology, Vol. 186, No. 1, 113-128 doi:10.1083/jcb.200811071
Ca2+ signaling evoked by activation of Na+ channels and Na+/Ca2+ exchangers is required for GABA-induced NG2 cell migration
Xiao-ping Tong, Xiang-yao Li, Bing Zhou, Wanhua Shen, Zhi-jun Zhang, Tian-le Xu, and Shumin Duan
Institute of Neuroscience and State Key Laboratory of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China
NG2 cells originate from various brain regions and migrate to their destinations during early development. These cells express voltage-gated Na+channels but fail to produce typical action potentials. The physiological role of Na+ channels in these cells is unclear. We found that GABA induces membrane depolarization and Ca2+ elevation in NG2 cells, a process requiring activation of GABAA receptors, Na+ channels, and Na+/Ca2+exchangers (NCXs), but not Ca2+ channels. We have identified a persistent Na+ current in these cells that may underlie the GABA-induced pathway ofprolonged Na+ elevation, which in turn triggers Ca2+ influx via NCXs. This unique Ca2+ signaling pathway is further shown to be involved in the migration of NG2 cells. Thus, GABAergic signaling mediated by sequential activation of GABAA receptors, noninactivating Na+ channels, and NCXs may play an important role in the development and function of NG2 glial cells in the brain.
