Sun Xue-Zhi, Takahashi Sentaro, Cui Chun, Zhang Rui, Sakata-Haga Hiromi, Sawada Kazuhiko, Fukui Yoshihiro
Environmental and Toxicological Sciences Research Group, National Institute of Radiological Sciences, Chiba, Chiba, Japan.
J Med Invest. 2002 Aug;49(3-4):97-110.
Neuronal migration is the critical cellular process which initiates histogenesis of cerebral cortex. Migration involves a series of complex cell interactions and transformation. After completing their final mitosis, neurons migrate from the ventricular zone into the cortical plate, and then establish neuronal lamina and settle onto the outermost layer, forming an "inside-out" gradient of maturation. This process is guided by radial glial fibers, requires proper receptors, ligands, other unknown extracellular factors, and local signaling to stop neuronal migration. This process is also highly sensitive to various physical, chemical and biological agents as well as to genetic mutations. Any disturbance of the normal process may result in neuronal migration disorder. Such neuronal migration disorder is believed as major cause of both gross brain malformation and more special cerebral structural and functional abnormalities in experimental animals and in humans. An increasing number of instructive studies on experimental models and several genetic model systems of neuronal migration disorder have established the foundation of cortex formation and provided deeper insights into the genetic and molecular mechanisms underlying normal and abnormal neuronal migration.
神经元迁移是启动大脑皮质组织发生的关键细胞过程。迁移涉及一系列复杂的细胞相互作用和转变。神经元在完成其最后的有丝分裂后,从脑室区迁移到皮质板,然后建立神经元层并定居在最外层,形成成熟的“由内向外”梯度。这个过程由放射状胶质纤维引导,需要适当的受体、配体、其他未知的细胞外因子以及局部信号来停止神经元迁移。这个过程对各种物理、化学和生物因素以及基因突变也高度敏感。正常过程的任何干扰都可能导致神经元迁移障碍。这种神经元迁移障碍被认为是实验动物和人类大脑严重畸形以及更特殊的脑结构和功能异常的主要原因。越来越多关于神经元迁移障碍实验模型和几个遗传模型系统的指导性研究为皮质形成奠定了基础,并为正常和异常神经元迁移的遗传和分子机制提供了更深入的见解。