Messersmith E K, Feller M B, Zhang H, Shatz C J
Howard Hughes Medical Institute, University of California at Berkeley 94720-3200, USA.
Mol Cell Neurosci. 1997;9(5-6):347-57. doi: 10.1006/mcne.1997.0646.
A variety of factors, from cell adhesion to changes in intracellular calcium, are thought to influence neuronal migration. Here we examine the possibility that calcium influx mediated via NMDA receptors regulates migration of neocortical neurons. We have examined the cytoarchitecture of the cortex in transgenic mice lacking functional NMDA receptors. Using cell birthdating techniques we found that cells in the developing neocortex of NMDAR-1 mutant mice have a distribution indistinguishable from that in animals with functional NMDA receptors, implying normal rates and routes of migration. These observations contrast with previous in vitro pharmacological studies of cerebellar granule cell migration, in which a role for NMDA receptors has been demonstrated. Thus, either different mechanisms are responsible for controlling neuronal migration in neocortex versus cerebellum or, more likely, neocortical neurons in NMDAR-1 mutant mice have acquired compensatory mechanisms for cell migration.
从细胞黏附到细胞内钙的变化等多种因素被认为会影响神经元迁移。在这里，我们研究了经由N-甲基-D-天冬氨酸（NMDA）受体介导的钙内流调节新皮层神经元迁移的可能性。我们检查了缺乏功能性NMDA受体的转基因小鼠的皮质细胞结构。使用细胞出生时间标记技术，我们发现NMDAR-1突变小鼠发育中的新皮层中的细胞分布与具有功能性NMDA受体的动物没有区别，这意味着迁移速率和路径正常。这些观察结果与先前关于小脑颗粒细胞迁移的体外药理学研究形成对比，在该研究中已证明NMDA受体发挥了作用。因此，要么是不同的机制控制着新皮层和小脑中的神经元迁移，要么更有可能的是，NMDAR-1突变小鼠中的新皮层神经元已经获得了细胞迁移的补偿机制。
