Godfraind C, Schachner M, Goffinet A M
University of Louvain Medical School, Developmental Neurology Unit, Brussels, Belgium.
Brain Res. 1988 Jul 1;470(1):99-111. doi: 10.1016/0165-3806(88)90205-2.
The expression of the cell adhesion molecules L1, J1 and N-CAM and their shared carbohydrate L2 was studied in the embryonic cerebral cortex of normal and reeler mutant mice using light and electron microscopic immunocytochemistry. Apart from a general delay in their appearance in the reeler cortex, the 4 antigens were present with a cellular distribution in both genotypes reflecting the anatomical characteristics of normal and mutant phenotypes. The cell surface glycoprotein L1 was exclusively expressed by neurons, particularly axons, but was never detected at sites of neuron-glia contact. L1 was accumulated in the marginal zone and subplate of the normal cortex and in the homologous layers of the reeler cortex. The secreted glycoprotein J1 was found on glia and neurons. Although initially present in regions of fiber outgrowth, J1 became characteristically excluded from the large fiber tracts at later stages. J1 mapped in the marginal zone and subcortical plate of the normal cortex and in the corresponding layers of the mutant cortex. N-CAM had a more ubiquitous distribution and was present in ventricular zones, particularly at early stages, as well as on glia and neurons and large fiber tracts at later developmental stages. The distribution of the L2 epitope was quite similar to that of the J1 molecule but remained present on large fiber tracts, like N-CAM and L1, also at later developmental stages. These comparative observations in normal and reeler mutant mice lend support to previous suggestions that L1, together with N-CAM, may play a role in the aggregation of neuronal cell bodies after migration and in the fasciculation of developing fiber bundles. They also point to a possible function of the extracellular matrix component J1 in the guidance or support of fiber outgrowth in large fiber tracts.
利用光镜和电镜免疫细胞化学技术，研究了正常和reeler突变小鼠胚胎大脑皮质中细胞黏附分子L1、J1和N-CAM及其共同碳水化合物L2的表达情况。除了在reeler皮质中出现普遍延迟外，这4种抗原在两种基因型中的细胞分布反映了正常和突变表型的解剖学特征。细胞表面糖蛋白L1仅由神经元表达，特别是轴突，但在神经元-神经胶质接触部位从未检测到。L1在正常皮质的边缘区和亚板以及reeler皮质的同源层中积累。分泌型糖蛋白J1在神经胶质细胞和神经元上被发现。尽管J1最初存在于纤维生长区域，但在后期它的特征是从大纤维束中排除。J1定位于正常皮质的边缘区和皮质下板以及突变皮质的相应层中。N-CAM分布更为广泛，在脑室区存在，特别是在早期阶段，在发育后期也存在于神经胶质细胞、神经元和大纤维束上。L2表位的分布与J1分子非常相似，但在发育后期也像N-CAM和L1一样存在于大纤维束上。在正常和reeler突变小鼠中的这些比较观察结果支持了先前的观点，即L1与N-CAM一起可能在神经元细胞体迁移后的聚集以及发育中的纤维束的成束过程中发挥作用。它们还指出细胞外基质成分J1在大纤维束中纤维生长的引导或支持方面可能具有的功能。
