園藝師都知道,,樹木只有定期修剪,,去掉某些枝條,剩下的才能長得更好,。這一規(guī)則同樣也適合大腦,。據(jù)美國物理學(xué)家組織網(wǎng)近日報(bào)道,位于意大利蒙特羅通多的歐洲分子生物實(shí)驗(yàn)室(EMBL)科學(xué)家發(fā)現(xiàn),,大腦中也有一種“園藝師”,,叫做小神經(jīng)膠質(zhì)細(xì)胞,它們能“修剪”神經(jīng)元之間的連接,,形成特定的網(wǎng)絡(luò)連接,。該發(fā)現(xiàn)有助于研究神經(jīng)發(fā)育紊亂方面的疾病,如孤獨(dú)癥,。論文近日發(fā)表在《科學(xué)》雜志網(wǎng)站上,。
“根據(jù)實(shí)驗(yàn)顯示,大腦要形成正確的網(wǎng)絡(luò)連接,,小神經(jīng)膠質(zhì)細(xì)胞非常關(guān)鍵,。”領(lǐng)導(dǎo)該研究的柯尼利斯·克洛斯說,,“它們會(huì)‘吃掉’神經(jīng)元突觸(突觸是神經(jīng)元之間的連接),留出空間給那些最有效的連接,,讓它們變得更強(qiáng)健,。”
小神經(jīng)膠質(zhì)細(xì)胞跟白細(xì)胞很像。白細(xì)胞能吞掉病原體和細(xì)胞殘骸,,而小神經(jīng)膠質(zhì)細(xì)胞會(huì)在腦受傷時(shí)起到同樣的作用,,吞掉那些已死的和快要死的神經(jīng)元??寺逅购屯吕蔑@微鏡觀察了小鼠的大腦,,結(jié)果在小神經(jīng)膠質(zhì)細(xì)胞中發(fā)現(xiàn)突觸蛋白,這表明小神經(jīng)膠質(zhì)細(xì)胞吞掉了它們,。為了進(jìn)一步探索小神經(jīng)膠質(zhì)細(xì)胞的功能,,他們引入了一種變異體,能降低小鼠腦發(fā)育過程中小神經(jīng)膠質(zhì)細(xì)胞的數(shù)量,。
“我們在這些小鼠腦中看到的情況跟某些人類孤獨(dú)癥患者很相似:神經(jīng)元之間有大量的連接,。”克洛斯說,“小神經(jīng)膠質(zhì)細(xì)胞所造成的變化是神經(jīng)發(fā)育紊亂的主要因素,,這些變化改變了大腦網(wǎng)絡(luò)線路,。”
實(shí)驗(yàn)所用的小神經(jīng)膠質(zhì)細(xì)胞限制型變異體只在短期內(nèi)有效,所以小神經(jīng)膠質(zhì)細(xì)胞最終還會(huì)增加,,此后小鼠大腦會(huì)建立起正確的連接,,但要比正常發(fā)育的小鼠建立連接延后。
研究人員表示,,目前他們正在研究這種延遲是否會(huì)長期存在,是否會(huì)影響小鼠的行為以及會(huì)影響它們的哪些行為,。(生物谷 Bioon.com)
doi:10.1016/j.cell.2005.08.020
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Synaptic Pruning by Microglia Is Necessary for Normal Brain Development
Paolicelli, Rosa C.; Bolasco, Giulia; Pagani, Francesca; Maggi, Laura; Scianni, Maria; Panzanelli, Patrizia; Giustetto, Maurizio; Ferreira, Tiago Alves; Guiducci, Eva; Dumas, Laura; Ragozzino, Davide; Gross, Cornelius T.
Microglia are highly motile phagocytic cells that infiltrate and take up residence in the developing brain, where they are thought to provide a surveillance and scavenging function. However, although microglia have been shown to engulf and clear damaged cellular debris after brain insult, it remains less clear what role microglia play in the uninjured brain. Here, we show that microglia actively engulf synaptic material and play a major role in synaptic pruning during postnatal development in mice. These findings link microglia surveillance to synaptic maturation and suggest that deficits in microglia function may contribute to synaptic abnormalities seen in some neurodevelopmental disorders