图片说明：缺少cdk5基因的新生神经细胞（绿色）形成异常树突，与先前已存在的神经细胞（红色）和神经胶质细胞（蓝色）成为一体。（图片来源：瑞士苏黎世联邦理工学院/Sebastian Jessberger）
美、德、瑞士等国科学家报告说，成体神经干细胞中的一个特定基因的失活，会使由这些干细胞形成的神经细胞在大脑中错误的位置形成连接。研究论文发表在11月11日的《PloS生物学》（PLoS Biology）上。
研究人员发现，一种名为cdk5的蛋白质对树突的正确建立和组成树突的细胞的恰当迁移都是必须的。研究小组领导人、美国索尔克生物学研究所的Fred H. Gage说：“令人惊奇的是，在成人海马组织中，缺少cdk5的新生粒细胞所形成的树突向错误的方向生长，事实上与‘错误’的细胞建立了神经连接。”
论文第一作者、瑞士苏黎世联邦理工学院副教授Sebastian Jessberger表示，“研究数据显示，没能正常生长的神经细胞可能也会与大脑连接起来并干扰正常的信息处理”，而且，“错误的神经连接并不会很快消失，甚至在1年以后，一些出现错误连接的神经细胞仍然留在了大脑的海马区。”
Gage说：“我们的研究表明，对于发展相应脑部疗法的研究人员来说，要保证疗法中涉及的细胞正确生长，这样才能形成合适的而不是混乱的神经连接。”
这一发现为脑损伤或神经退行性疾病疗法的研究人员提供了非常有价值的信息，可能会对神经组织移植产生深远的影响。（生物谷Bioon.com）
生物谷推荐原始出处：
PLoS Biology，doi:10.1371/journal.pbio.0060272，Sebastian Jessberger，Fred 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.
