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目的兴奋毒性是导致中枢神经元死亡的主要因素之一。为此,本实验旨在形态学探察证实纹状体不同类型中间神经元对兴奋毒性损害因素的特征性反应。方法借助喹啉酸(QA)兴奋毒性损伤模型、组织化学和免疫组织化学方法探察证实纹状体损伤区不同类型中间神经元的形态和数量变化。实验数据以SPSS软件统计分析。结果①纹状体损伤区神经元的丢失显示不同的形式;即在损伤灶中央区绝大部分神经元均显著减少;在过渡区中等大小的神经元严重损害,一些大体积、组织化学深染色的神经元仍然幸存。②五种中间神经元的免疫组化结果显示在纹状体损伤中央区中间神经元完全丢失,但具有特征性变化的是过渡区,该区域中间神经元胞体数量变化不明显,而轴突出现大量的增生性变化,尤其是Cr最为显著,其表现为密集纤维网络的形成及大量的串珠样变化。结论纹状体中间神经元对兴奋毒性损伤的反应程度与受累区域相关,损伤过渡区中间神经元轴突形态和数量显示增生特征性的变化。结果提示过渡区可能是决定中间神经元生存和死亡的关键部位,以及中间神经元可能牵涉到纹状体兴奋毒性损伤的病理机制。
The purpose of excitotoxicity is one of the main factors leading to the death of central neurons. For this reason, the present study aimed to morphologically investigate the characteristic responses of different types of interneurons in striatum to the excitotoxicity. Methods The morphological and quantitative changes of different types of interneurons in injured area of striatum were detected by means of excitotoxicity injury model of QA, histochemistry and immunohistochemistry. Experimental data to SPSS software statistical analysis. Results ① The loss of neurons in the injured area of striatum showed different forms; that is, most of the neurons in the central lesion were significantly reduced; neurons of intermediate size in the transitional area were severely damaged; some large-volume, histochemical deep staining The neurons still survive. ② The results of immunohistochemistry of the five kinds of interneurons showed that the neurons in the central area of striatum were completely lost, but the transitional areas with characteristic changes were obvious. The number of the neurons in the middle neurons did not change obviously, but the axons appeared A large number of proliferative changes, especially the most significant Cr, manifested as dense fiber network formation and a large number of beaded changes. Conclusions The response of striatal interneurons to excitotoxicity is related to the affected area. The morphology and number of axons in the intermediate neurons in the transitional area show the characteristic changes of hyperplasia. The results suggest that the transition zone may be the key site that determines the survival and death of interneurons, and the pathological mechanism that interneurons may involve excitotoxic damage of striatum.