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目的探讨生酮饮食对海藻酸致大鼠海马突触重建和G luR5表达的影响机制。方法以海藻酸(KA)致的幼鼠为研究对象,采用Timm′s染色和尼氏染色,观察经不同饮食处理的动物海马结构和癫行为的变化;并用W estern B lot和RT-PCR法检测海马G luR5及其mRNA的表达。结果生酮饮食组动物自发性反复惊厥的次数(1.40±1.03)次,明显少于正常饮食组(7.36±3.75)次。KA致大鼠海马齿状回内分子层异常Timm′s染色颗粒的平均A值均显著高于非致组,但生酮饮食组和正常饮食组间则无明显差异;各组动物CA3区锥体细胞层及始层的Timm′s染色颗粒以及海马门区和CA1、CA3区神经元的平均A值未见明显差异。KA致后生酮饮食组大鼠海马G luR5的表达[(189.38±40.03)/mg总蛋白]明显高于正常饮食组[(128.79±46.51)/mg总蛋白],但两组间G luR5mRNA比较,差异无统计学意义。结论苔藓纤维发芽可能是KA致动物癫产生的原因,酮食疗法对KA致大鼠确有抗癫作用,其抗癫机制可能与增加幼年大鼠CA1区中间神经元G luR5的表达,使海马内抑制性突触传递增强,进而阻止癫活动扩散有关。
Objective To investigate the mechanism of ketogenic diet on the synaptic remodeling and G luR5 expression in rat hippocampus induced by alginic acid. Methods Kindergarten mice induced by alginic acid (KA) were used as experimental objects. The changes of hippocampal structure and epilepsy in different diets were observed by Timm’s staining and Nissl’s staining. The hippocampal G luR5 and its mRNA expression were detected. Results The frequency of spontaneous recurrent seizures (1.40 ± 1.03) in the ketogenic diet group was significantly less than that in the normal diet group (7.36 ± 3.75). The mean A value of Timm’s stained granules in KA-induced dentate gyms was significantly higher than that in non-induced rats, but there was no significant difference between ketogenic diet group and normal diet group There was no significant difference in the average A value of Timm’s staining granules in the somatic and basal lamina, as well as in the hippocampus and CA1 and CA3 neurons. Compared with the normal diet group [(128.79 ± 46.51) / mg total protein], the expression of G luR5 in the hippocampus of KA induced ketogenic diet group [(189.38 ± 40.03) / mg total protein] was significantly higher than that of the normal diet group The difference was not statistically significant. Conclusion Mossy fiber sprouting may be the cause of KA-induced epilepsy in rats. Ketone therapy may have antiepileptic effect on KA-induced rats. The antiepileptic mechanism may be related to increasing the expression of GluR5 in the interneurons of CA1 in young rats, Increased inhibitory synaptic transmission, thereby preventing the spread of epilepsy activity.