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大鼠三叉神经痛动物模型三叉神经根进入区神经胶质可塑性研究。

Glial Plasticity in the Trigeminal Root Entry Zone of a Rat Trigeminal Neuralgia Animal Model.

机构信息

Department of Human Anatomy, Histology and Embryology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, 350122, China.

Key Laboratory of Brain Aging and Neurodegenerative Diseases of Fujian Province, Fuzhou, 350122, China.

出版信息

Neurochem Res. 2019 Aug;44(8):1893-1902. doi: 10.1007/s11064-019-02824-2. Epub 2019 Jun 17.

Abstract

The trigeminal root entry zone (TREZ) is the transitional zone of central and peripheral tissue compartments in the trigeminal root. Microvascular compression on the TREZ is the main etiology of most idiopathic trigeminal neuralgia (TN) patients. However, the pathogenesis of TN is still uncertain. To investigate the glial plasticity changes in oligodendrocytes, Schwann cells, astrocytes and microglia/macrophages in the TREZ in TN, immunohistochemical staining and Western blot methods were performed in rats with TN induced by compression injury. The results showed that mechanical compression injury in the trigeminal nerve of the TN rats induced glial plasticity in the TREZ, which dynamically changed the glial interface of the CNS-PNS transitional zone. Additionally, glial fibrillary acidic protein (GFAP)-immunoreactive astrocyte processes significantly proliferated and extended distally from the central region to the peripheral side of the TREZ after nerve compression injury in the TN group. Moreover, the expression of p75 in Schwann cells was upregulated on the peripheral side of the TREZ, and activated Iba-1-immunoreactive microglia/macrophages were observed on both sides of the TREZ. A significantly higher number of Schwann cells, astrocytes and microglia/macrophages were found in the TN group than in the sham operation group (p < 0.05). In conclusion, mechanical compression injury in the TN rats activated various glial cells, including oligodendrocytes, astrocytes, Schwann cells and microglia/macrophages, in the CNS-PNS transitional zone of TREZ. Changes in glial cell plasticity in the TREZ after compression injury might be involved in TN pathogenesis.

摘要

三叉神经根入口区(TREZ)是三叉神经根中央和周围组织隔室的过渡区。TREZ 上的微血管压迫是大多数特发性三叉神经痛(TN)患者的主要病因。然而,TN 的发病机制仍不确定。为了研究 TN 患者 TREZ 中少突胶质细胞、施万细胞、星形胶质细胞和小胶质细胞/巨噬细胞的神经胶质可塑性变化,采用压迫损伤法建立大鼠 TN 模型,用免疫组织化学染色和 Western blot 方法进行检测。结果显示,TN 大鼠三叉神经的机械性压迫损伤诱导了 TREZ 中的神经胶质可塑性,从而使中枢神经系统-周围神经系统过渡区的神经胶质界面发生动态变化。此外,在 TN 组神经压迫损伤后,GFAP 免疫反应性星形胶质细胞突起从中央区域向 TREZ 的外周侧显著地延伸和增殖。此外,TREZ 外周侧施万细胞的 p75 表达上调,TREZ 两侧均观察到激活的 Iba-1 免疫反应性小胶质细胞/巨噬细胞。与假手术组相比,TN 组的施万细胞、星形胶质细胞和小胶质细胞/巨噬细胞数量显著增加(p<0.05)。总之,TN 大鼠的机械性压迫损伤激活了 TREZ 中中枢神经系统-周围神经系统过渡区的各种神经胶质细胞,包括少突胶质细胞、星形胶质细胞、施万细胞和小胶质细胞/巨噬细胞。TREZ 中神经胶质细胞可塑性在压迫损伤后的改变可能与 TN 的发病机制有关。

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