大鼠纹状体中间神经元对兴奋毒性损伤特征性反应的形态学证实

Morphological evidence for the specific response of striatal interneurons to excitotoxicity in rats

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。

Objective Excitotoxicity is one of the main factors that leads to the death of central neurons.This present study designed to confirm the characteristic response of different striatal interneurons types to the damage of excitotoxicity.Methods QA excitotoxicity model,histochemistry and immunohistochemistry were used to detect the change in morphology and number of different striatal interneurons types in injured striatum.Experimental data were analyzed with SPSS software.Results ①The loss of neurons in injured striatum showed different patterns.Histochemistry stain displayed a complete loss of neurons in the core,but in the transition zone,medium neurons decreased obviously with some big neurons survived.②Immuntochemistry stain of the five interneuron types showed no positive cells in the lesions core,specific changes happened in the transition zone where there was no obvious change in the soma of the five interneuron types,but their processes showed different extents of hyperplasia,especially for Cr＋ axons,which formed intensive fiber network and numerous varicosities.Conclusion The damaged extent of striatal interneurons to excitotoxicity was related to the injured region,the morphology and number of axons showed characteristic hyperplasia in the transition zone.The results suggest that the transition zone be the key region to decide survival or death of satriatal neurons,and interneurons be involved in the pathogenesis of striatal excitotoxicity.