据9月16日Nature杂志网络版的一篇研究报告，耶鲁大学的研究人员发现，大脑皮层不同神经元混合形成纵向柱状排列的分子机制。
大脑皮层进行信息处理依赖于一组纵向柱状排列的神经元。一旦这些神经元的数量和种类发生错误，则会引起认知能力障碍，如导致自闭症和智力迟钝等。但一直以来，科学家对这种柱状排列的混合神经元的分子机制不甚了解。
在这篇由Pasko Rakic教授主持的课题组中，研究人员利用先进的分子技术表明，在神经细胞迁移过程中，柱状排列的混合神经元依赖于两种基因——A-型Eph受体以及ephrin-As配体基因的表达水平，ephrin-As配体结合到A-型Eph受体上。研究发现，当小鼠缺少配体或受体的情况下，神经细胞将不能横向迁移到柱状的合适位置。
据第一作者Masaaki Torii介绍，他发现这两种基因所控制的神经细胞的横向迁移在正常的大脑皮质的发育过程中起着总要的作用。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature 16 September 2009 | doi:10.1038/nature08362
Integration of neuronal clones in the radial cortical columns by EphA and ephrin-A signalling
Masaaki Torii1,2, Kazue Hashimoto-Torii1, Pat Levitt2 & Pasko Rakic1
1 Department of Neurobiology and Kavli Institute for Neuroscience, Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06510, USA
2 Zilkha Neurogenetic Institute and Department of Cell and Neurobiology, Keck School of Medicine of USC, Los Angeles, California 90089, USA
The cerebral cortex is a laminated sheet of neurons composed of the arrays of intersecting radial columns1, 2, 3. During development, excitatory projection neurons originating from the proliferative units at the ventricular surface of the embryonic cerebral vesicles migrate along elongated radial glial fibres4 to form a cellular infrastructure of radial (vertical) ontogenetic columns in the overlaying cortical plate5. However, a subpopulation of these clonally related neurons also undergoes a short lateral shift and transfers from their parental to the neighbouring radial glial fibres6, and intermixes with neurons originating from neighbouring proliferative units5, 7. This columnar organization acts as the primary information processing unit in the cortex1, 8, 9. The molecular mechanisms, role and significance of this lateral dispersion for cortical development are not understood. Here we show that an Eph receptor A (EphA) and ephrin A (Efna) signalling-dependent shift in the allocation of clonally related neurons is essential for the proper assembly of cortical columns. In contrast to the relatively uniform labelling of the developing cortical plate by various molecular markers and retrograde tracers in wild-type mice, we found alternating labelling of columnar compartments in Efna knockout mice that are caused by impaired lateral dispersion of migrating neurons rather than by altered cell production or death. Furthermore, in utero electroporation showed that lateral dispersion depends on the expression levels of EphAs and ephrin-As during neuronal migration. This so far unrecognized mechanism for lateral neuronal dispersion seems to be essential for the proper intermixing of neuronal types in the cortical columns, which, when disrupted, might contribute to neuropsychiatric disorders associated with abnormal columnar organization8, 10.
