慢性癫痫模型动物海马内GABA能神经元的超微结构改变

ULTRASTRUCTURAL CHANGES OF HIPPOCAMPAL GABA-ERGIC NEURONS IN CHRONIC EPILEPTIC MODEL ANIMAL

用马桑内酯诱发小鼠慢性癫痫模型，借助免疫电镜方法对海马的ＧＡＢＡ能神经元的超微结构进行观察，可见小鼠海马内ＧＡＢＡ免疫反应阳性神经元弥散分布于除锥体细胞层和颗粒细胞层外的各部。慢性癫痫小鼠海马内的ＧＡＢＡ免疫反应阳性神经元胞体和末梢均呈现程度不同的结构损伤，包括线粒体肿胀、细胞器崩解和神经末梢变性。ＧＡＢＡ样轴突末梢可与免疫反应阴性的树突构成传出性轴－树突触，也可接受免疫反应阴性轴突末梢的传入性轴－轴突触。在模型动物海马内的非ＧＡＢＡ能神经元结构与正常对照动物者相似，但线粒体有增多趋势，甚至成团聚集于神经末梢，未见结构损伤。此外，在癫痫小鼠，ＧＡＢＡ免疫反应产物还分布于星形胶质细胞和毛细血管内皮细胞胞浆内。以上实验结果表明：在慢性癫痫时ＧＡＢＡ在海马的含量减少，而非ＧＡＢＡ能神经元的代谢和活性增强，这些变化可能与癫痫的发病机理有关。

The chronic epileptic model was induced by coriaria lactone in mice. By means of immunoelectron microscopic method,the ultrastructure of hippocampal GABA-ergic neurons was observed.The hippocampal GABA immunoreactive(IR)neurons distributed diffusely in all(except pyramidal and granular)layers,The hippocampaI GABA-IR neuronal perikarya and terminals in chronic epileptic mice showed various degrees of damages including mitochondrial swelling,breakdown of organelles and terminal degeneration,The GABA-IR axon terminals formed efferent axo-dendritic synapses with GABA-negative dendrites and received afferent axoaxonic synapses with GABA-negative axon terminals,In hippocampus of model animal,the ultrastructure of non-GABA-ergic neurons appeared to be similar to control animal,but mitochondria tended to increased and even accumulated in the nerve terminal with normal structure.In addition,GABA-IR products also distributed in astrocytes and capillary endothelia of model mice,The above mentioned results indicated that in chronic epilepsy the GABA content in hippocampus decreased,whereas the metabolism and activity of non-GABA-ergic neurons enhanced.All of these changes might be related to pathogenesis of epilepsy.