圖片說(shuō)明：缺少cdk5基因的新生神經(jīng)細(xì)胞（綠色）形成異常樹(shù)突，與先前已存在的神經(jīng)細(xì)胞（紅色）和神經(jīng)膠質(zhì)細(xì)胞（藍(lán)色）成為一體。（圖片來(lái)源：瑞士蘇黎世聯(lián)邦理工學(xué)院/Sebastian Jessberger）
美,、德,、瑞士等國(guó)科學(xué)家報(bào)告說(shuō)，成體神經(jīng)干細(xì)胞中的一個(gè)特定基因的失活，會(huì)使由這些干細(xì)胞形成的神經(jīng)細(xì)胞在大腦中錯(cuò)誤的位置形成連接,。研究論文發(fā)表在11月11日的《PloS生物學(xué)》（PLoS Biology）上。
研究人員發(fā)現(xiàn),，一種名為cdk5的蛋白質(zhì)對(duì)樹(shù)突的正確建立和組成樹(shù)突的細(xì)胞的恰當(dāng)遷移都是必須的,。研究小組領(lǐng)導(dǎo)人、美國(guó)索爾克生物學(xué)研究所的Fred H. Gage說(shuō)：“令人驚奇的是,，在成人海馬組織中,，缺少cdk5的新生粒細(xì)胞所形成的樹(shù)突向錯(cuò)誤的方向生長(zhǎng)，事實(shí)上與‘錯(cuò)誤’的細(xì)胞建立了神經(jīng)連接,。”
論文第一作者,、瑞士蘇黎世聯(lián)邦理工學(xué)院副教授Sebastian Jessberger表示，“研究數(shù)據(jù)顯示,，沒(méi)能正常生長(zhǎng)的神經(jīng)細(xì)胞可能也會(huì)與大腦連接起來(lái)并干擾正常的信息處理”,，而且，“錯(cuò)誤的神經(jīng)連接并不會(huì)很快消失,，甚至在1年以后,，一些出現(xiàn)錯(cuò)誤連接的神經(jīng)細(xì)胞仍然留在了大腦的海馬區(qū)。”
Gage說(shuō)：“我們的研究表明,，對(duì)于發(fā)展相應(yīng)腦部療法的研究人員來(lái)說(shuō),，要保證療法中涉及的細(xì)胞正確生長(zhǎng)，這樣才能形成合適的而不是混亂的神經(jīng)連接,。”
這一發(fā)現(xiàn)為腦損傷或神經(jīng)退行性疾病療法的研究人員提供了非常有價(jià)值的信息,，可能會(huì)對(duì)神經(jīng)組織移植產(chǎn)生深遠(yuǎn)的影響。（生物谷Bioon.com）
生物谷推薦原始出處：
PLoS Biology,，doi:10.1371/journal.pbio.0060272，Sebastian Jessberger,，F(xiàn)red H. Gage
Cdk5 Regulates Accurate Maturation of Newborn Granule Cells in the Adult Hippocampus
Sebastian Jessberger1,2*, Stefan Aigner1, Gregory D. Clemenson Jr.1, Nicolas Toni1, D. Chichung Lie1,3, ?zlem Karalay2, Rupert Overall4, Gerd Kempermann4, Fred H. Gage1*
1 Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California, United States of America, 2 Institute of Cell Biology, Department of Biology, ETH Zurich, Zurich, Switzerland, 3 Helmholtz Zentrum München, German Research Center for Environmental Health, Munich, Germany, 4 Center for Regenerative Therapies (CRTD), Dresden, Germany
Newborn granule cells become functionally integrated into the synaptic circuitry of the adult dentate gyrus after a morphological and electrophysiological maturation process. The molecular mechanisms by which immature neurons and the neurites extending from them find their appropriate position and target area remain largely unknown. Here we show that single-cell–specific knockdown of cyclin-dependent kinase 5 (cdk5) activity in newborn cells using a retrovirus-based strategy leads to aberrant growth of dendritic processes, which is associated with an altered migration pattern of newborn cells. Even though spine formation and maturation are reduced in cdk5-deficient cells, aberrant dendrites form ectopic synapses onto hilar neurons. These observations identify cdk5 to be critically involved in the maturation and dendrite extension of newborn neurons in the course of adult neurogenesis. The data presented here also suggest a mechanistic dissociation between accurate dendritic targeting and subsequent synapse formation.
