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目的:利用红藻氨酸(kainate,KA)致大鼠复杂部分性发作模型,观察海马及齿状回等易损脑区N-甲基-D-门冬氨酸受体1亚单位(NMDAR_1)的变化,以期进一步探明迷走神经刺激治疗癫(疒间)的作用机制。方法:免疫细胞化学法。结果:正常大鼠NMDAR_1阳性结构可见于海马各区及齿状回;KA给药后1h海马CA1、CA3、齿状回NMDAR_1的密度开始增高;3h达高峰,以后逐渐下降,24h后基本恢复正常;预先给予左侧迷走神经电刺激治疗的大鼠相应脑区NMDAR_1密度较KA致(疒间)组明显降低,具有统计学差异。结论:迷走神经刺激抑制癫(疒间)发作可能是通过降低易损脑区神经元NMDAR_1活性而发挥作用的。
OBJECTIVE: To explore the mechanism of complex partial seizures induced by kainate (KA) in rats and observe the changes of N-methyl-D-aspartate receptor subunit 1 (NMDAR_1 ) Changes in order to further explore the vagus nerve stimulation in the treatment of epilepsy (pterygium) mechanism of action. Methods: Immunocytochemistry. Results: The normal structure of NMDAR_1 in normal rats was found in hippocampus and dentate gyrus. The density of hippocampal CA1 and CA3 and dentate gyrus NMDAR_1 began to increase at 1h after KA administration, reached peak at 3h, then decreased gradually and returned to normal after 24h. The density of NMDAR_1 in the corresponding brain regions in the left vagus nerve stimulation group was significantly lower than that in the KA group (P <0.05), with statistical difference. Conclusion: The vagus nerve stimulation can inhibit the onset of epileptogenesis in the brain by decreasing NMDAR 1 activity in the vulnerable neurons.