【摘要】 目的:探讨神经肽Y(neuropeptide Y,NPY)中间神经元在颞叶癫痫的发生和自我修复中的作用。方法:建立匹罗卡品致痫模型,应用免疫组织化学技术动态观察大鼠海马NPY中间神经元的数目变化及其轴突出芽。结果:实验组大鼠腹腔注射氯化锂-匹罗卡品后,癫痫持续状态(status epilepticus,SE)诱发成功率为92.9%,死亡率19.2%。免疫组织化学结果显示,实验组大鼠海马门区NPY中间神经元数目在SE后下降,至7d时降至最低(P<0.01),慢性期开始恢复,SE后60d时NPY神经元数目与对照组相比仍有减少(P<0.05);CA区域除SE后7dCA3区NPY神经元数目稍减少外(P<0.05),其余时间点均无明显变化(P>0.05);SE后30d齿状回分子层可见增多的NPY阳性纤维。结论:NPY中间神经元在不同部位不同时段对颞叶癫痫所致损伤的敏感性不同,NPY中间神经元的缺失在颞叶癫痫发生中起重要作用,NPY中间神经元的轴突出芽在颞叶癫痫的自我修复中起作用。更多还原

【Abstract】 Objective To investigate the role of neuropeptide Y(NPY) positive interneurons in the generation and compensation of temporal lobe epilepsy.Methods Pilocarpine-induced rat model was founded.Immunohistochemistry was used to observe the number changes and axonal sprouting of NPY interneurons at different time points in the hippocampus of rats.Results After lithium-chloride and pilocarpine administration,92.9% rats were induced status epilepticus(SE) successfully,and the mortality rate was 19.2%.In the experimental group,the number of NPY positive neurons decreased in the hilus of the hippocampus,and was least on 7 d after the SE(P<0.01).In the chronic phase,the number of hilus NPY neurons partially recovered,but was still less than the number in the control group on 60 d after the SE(P<0.05).No evident changes of the number of NPY neurons existed in CA domains(P>0.05) except the loss of them in CA3 area on 7 d after the SE(P>0.05).Increased NPY positive fibers could be seen in the molecular layer of the dentate gyrus on 30 d after the SE.Conclusion NPY interneurons have different sensitivities to the injuries induced by seizures at different time points and domains.Loss of NPY interneurons plays an important role in the generation of temporal lobe epilepsy,while axonal sprouting of them may play a significant role in the compensation of temporal lobe epilepsy.更多还原