首页> 外文期刊>The European Journal of Neuroscience >Aberrant trajectory of entorhino-dentate axons in the mutant Shaking Rat Kawasaki: a Dil-labelling study.
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Aberrant trajectory of entorhino-dentate axons in the mutant Shaking Rat Kawasaki: a Dil-labelling study.

机译:突变的摇晃大鼠川崎中的内嗅齿轴突的异常轨迹:一项Dil标记研究。

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摘要

The Shaking Rat Kawasaki (SRK) is a neurological mutant that exhibits abnormalities of cell migration and lamination, with many similarities to the mouse reeler mutant. We recently used lamina-specific antibody staining to show that despite severe aberrations in the laminar organization of the SRK dentate gyrus, the entorhinal terminal field in the outer dentate molecular layer appeared relatively normal (Woodhams & Terashima, 1999, J. Comp. Neurol. 409 p57). However, neurofilament immunostaining suggested that entorhino-dentate afferents take an abnormal trajectory in reaching their appropriate targets, the granule cells dendrites. In the present study, anterograde tracing with the carbocyanine dye 1, 1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate (DiI) has been used to delineate directly the path that entorhinal axons take to the dentate gyrus, confirming that in SRK entorhinal axons do indeed reach their appropriate terminal fields in the molecular layer, with laminar segregation between projections from the lateral and medial entorhinal cortices. However, these fibres fail to cross the hippocampal fissure between the subiculum and the dentate gyrus, coursing instead parallel to it until they curve round the deepest point of the fissure in field CA3. Similar findings were seen in the murine reeler mutant. Insertion of DiI crystals into the entorhinal cortex of neonatal rats also retrogradely labelled the developmentally transient Cajal-Retzius cells at the hippocampal fissure; these survive for longer in SRK than in normal littermates. The presence of a marked astrogliosis at the SRK hippocampal fissure may play a part in determining the abnormal trajectory taken by entorhino-dentate afferents in this mutant.
机译:摇床川崎(SRK)是一种神经系统突变体,表现出细胞迁移和层压异常,与小鼠reeler突变体有很多相似之处。我们最近使用层特异性抗体染色显示,尽管SRK齿状回的层状组织存在严重畸变,但齿状外分子层的内啡肽终末域似乎相对正常(Woodhams&Terashima,1999,J.Comp.Neurol。 409 p57)。然而,神经丝免疫染色提示,有牙本质的传入细胞在到达其适当的靶标时会出现异常轨迹,颗粒细胞会发生树突。在本研究中,使用碳花色素1、1'-二十八烷基-3,3,3',3'-四甲基吲哚碳菁高氯酸盐(DiI)进行顺向性示踪已直接描绘出内啡肽轴突进入齿状回的路径,证实在SRK中,内嗅轴突确实确实到达了分子层中的适当末端区域,并且从内外侧皮质和内侧内嗅皮质的突起之间层流隔离。但是,这些纤维无法穿过下丘脑和齿状回之间的海马裂隙,而是平行于其漂移,直到它们围绕场CA3中的裂隙的最深点弯曲为止。在鼠re变种中也发现了类似的发现。在新生大鼠的内嗅皮层中插入DiI晶体也逆行标记了海马裂隙中发育短暂的Cajal-Retzius细胞;与正常同窝仔相比,它们在SRK中存活的时间更长。 SRK海马裂隙中明显的星形胶质细胞增生的存在可能在确定该突变体的内嗅齿传入神经所采取的异常轨迹中起作用。

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