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为探讨听源性惊厥点燃对突触可塑性的影响，采用免疫细胞化学方法结合体视学分析，研究了Ｗｉｓｔａｒ种系的听源性惊厥易感大鼠（Ｐ７７ＰＭＣ）惊厥和点燃后海马结构内突触素ｐ３８表达的差异。结果显示：（１）Ｐ７７ＰＭＣ大鼠１次惊厥后，海马结构内ｐ３８免疫反应产物呈明显的板层样分布；（２）Ｐ７７ＰＭＣ大鼠点燃后，ｐ３８免疫反应产物的定位分布与１次惊厥后相比较，没有明显改变，但是，ｐ３８免疫反应产物的密度普遍增加，特别是在海马ＣＡ３区苔藓纤维层和齿状回分子层内带，ｐ３８免疫反应产物的光密度值显著增加（Ｐ＜０．０５）。结果表明，听源性惊厥点燃能够诱导海马结构内ｐ３８表达增加。本文讨论了ｐ３８表达增加的可能机制及其生物学意义。
To investigate the effect of auditory convulsion-induced synaptic plasticity on synaptic plasticity, we used immunocytochemistry combined with stereological analysis to study the effects of convulsions and ignition of hippocampal formation after convulsions in the Wistar germ-line etiology-induced seizure (P77PMC) Differences in the expression of tacrolimus p38. The results showed that: (1) The p38 immunoreactive products in the hippocampal formation were obviously lamella-like distribution in P77PMC rats after a seizure; (2) After the P77PMC rats were ignited, the localization of the p38 immunoreactive products and the post-convulsion However, there was a general increase in the density of the p38 immune response product, especially in the moss fiber layer and dentate gyrus in the CA3 region of the hippocampus, the optical density of the p38 immunoreactive product increased significantly (P <0 .05). The results show that auditory convulsion can induce p38 expression in hippocampal formation increased. This article discusses the possible mechanism of increasing p38 expression and its biological significance.