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甲状腺功能减退对大鼠海马结构中神经胶质细胞发育的影响:一项免疫细胞化学研究。

Effect of thyroid deficiency on the development of glia in the hippocampal formation of the rat: an immunocytochemical study.

作者信息

Rami A, Rabié A

机构信息

CNRS UA 1197, Laboratoire de Neurobiologie Endocrinologique, Université des Sciences et Techniques du Languedoc, Montpellier, France.

出版信息

Glia. 1988;1(5):337-45. doi: 10.1002/glia.440010506.

DOI:10.1002/glia.440010506
PMID:2976395
Abstract

The development of glia in the hippocampal formation of normal and hypothyroid rats was studied using immunocytochemical staining for either glial fibrillary acidic protein (GFAP) or vimentin. Light microscopy showed lower GFAP immunoreactivity in the radial glial processes of young hypothyroid rats compared to normal animals. These processes followed the known path of neuroblast migration toward the proliferative zone of the dentate gyrus until the end of the 1st postnatal week. Vimentin immunoreactivity showed that the glial processes were present and therefore immature at least with respect to their cytoskeletal composition. We propose that this early defect in the maturation of the radial glial fibers accounts for the final deficit in the granule cells of the dentate gyrus. Later in development, thyroid deficiency also reduced the density and number of GFAP-labeled astrocytes and the growth of their processes. This observation is in complete disagreement with the glial hypertrophy induced by thyroid deficiency in the cerebellum. The considerably increased histogenetic cell death observed in the cerebellum of young hypothyroid rats could in turn induce glial hypertrophy, whereas the hippocampal formation, where a normal low number of cell deaths is observed, is only subjected to the general depressive effect of thyroid deficiency on cell maturation.

摘要

利用针对胶质纤维酸性蛋白(GFAP)或波形蛋白的免疫细胞化学染色,研究了正常大鼠和甲状腺功能减退大鼠海马结构中胶质细胞的发育情况。光学显微镜显示,与正常动物相比,幼年甲状腺功能减退大鼠的放射状胶质细胞突起中的GFAP免疫反应性较低。这些突起沿着已知的神经母细胞迁移路径朝向齿状回的增殖区,直至出生后第一周结束。波形蛋白免疫反应性表明胶质细胞突起存在,因此至少就其细胞骨架组成而言是不成熟的。我们认为,放射状胶质纤维成熟的这种早期缺陷是齿状回颗粒细胞最终出现缺陷的原因。在发育后期,甲状腺功能减退也会降低GFAP标记的星形胶质细胞的密度和数量及其突起的生长。这一观察结果与甲状腺功能减退在小脑中诱导的胶质细胞肥大完全不同。在幼年甲状腺功能减退大鼠的小脑中观察到的组织发生性细胞死亡显著增加,进而可能诱导胶质细胞肥大,而在海马结构中,观察到正常情况下细胞死亡数量较少,仅受到甲状腺功能减退对细胞成熟的一般抑制作用。

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