Postnatal Development of Entorhinodentate Projection of the Reeler Mutant Mouse
Postnatal Development of Entorhinodentate Projection of the Reeler Mutant Mouse
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DOI：
10.1159/000096211
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发表时间：
2006-12
影响因子：
2.9
通讯作者：
D. Muraoka;Y. Katsuyama;S. Kikkawa;T. Terashima
中科院分区：
文献类型：
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作者：
D. Muraoka;Y. Katsuyama;S. Kikkawa;T. Terashima
通过向成年野生型小鼠和reeler小鼠的内嗅皮层注射生物素葡聚糖胺，对内齿突轴突进行顺行标记，以明确reeler小鼠内嗅投射的过程和末端是否正常。我们发现，在reeler小鼠中，来自内嗅皮层的生物素葡聚糖胺标记的内嗅齿状纤维在海马裂缝周围弯曲而不是穿过它，而在野生型小鼠中，它们以穿透途径穿过裂缝。接下来，我们基于层粘连蛋白和胶质纤维酸性蛋白（GFAP）免疫组化检测了未成熟内齿突突起的碳青素染料（DiI）标记和出生后早期海马裂的发育变化。在出生后第1天将DiI注射到野生型和reeler小鼠的内嗅区，导致先锋轴突通过海马裂隙的顺行标记。然而，在reeler小鼠中，跟随轴突不能穿过海马裂缝，而在正常对照中，许多dii标记的轴突继续穿过裂缝。GFAP免疫组化结果显示，野生型和reeler小鼠出生时，沿海马裂均有大量GFAP免疫阳性的星形胶质细胞。在野生型小鼠中，裂缝附近的gap阳性神经元数量在出生后早期逐渐减少，而在reeler小鼠中，许多gap阳性星形胶质细胞在那里继续积累。reeler小鼠的星形胶质细胞形成的这种屏障可能会阻碍从内嗅皮层产生的跟随轴突通过海马裂隙向内生长，导致该突变体的内嗅齿状轴突发育异常。
We anterogradely labeled entorhinodentate axons by the injection of biotin dextran amine into the entorhinal cortex of adult wildtype and reeler mice to clarify whether the course and terminal endings of the reeler entorhinal projection are normal or not. We found that in the reeler mouse, biotin dextran amine-labeled entorhinodentate fibers arising from the entorhinal cortex curved around the hippocampal fissure instead of crossing it, whereas in the wildtype mouse, they crossed the fissure as a perforant pathway. Next, we examined carbocyanine dye (DiI) labeling of the immature entorhinodentate projection and the developmental changes of the hippocampal fissure during early postnatal days based on the laminin and glial fibrillary acidic protein (GFAP) immunohistochemistry. Injection of DiI into the entorhinal area of the wildtype and reeler mice at postnatal day 1 resulted in anterograde labeling of pioneer axons passing through the hippocampal fissure. However, follower axons could not penetrate through the hippocampal fissure in reeler mice, whereas in the normal controls, many DiI-labeled axons continued to pass through the fissure. GFAP immunohistochemistry demonstrated that GFAP-immunopositive astrocytes were abundant along the hippocampal fissure both in the wildtype and reeler mice at birth. In the wildtype mouse, GFAP-positive neurons nearby the fissure were decreasing in number during the early postnatal days, whereas in the reeler mouse, many GFAP-positive astrocytes were continuing to accumulate there. This barrier made of astrocytes in the reeler mouse may obstruct the ingrowth of the follower axons arising from the entorhinal cortex through the hippocampal fissure, resulting in the abnormal course of the entorhinodentate axons in this mutant.