迷走神经刺激对红藻氨酸致癎大鼠海马及齿状回NMDAR_1的影响

The Effect of Vagus Nerve Stimulation on NMDAR_1 in Hippocampus of the Kainate Induced Epileptic Rat

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。

ve: Using the rat complex partial seizure model induced by kainate, we evaluated the distribution and density of N-methyl-D-aspartate receptor type I (NMDAR1) in the vulnerable brain areas including hippocampus and dentate gyrus, and aimed to find out the antiepileptic mechanisms of vagus nerve stimulation (VNS). Methods: Using immunohistochemistry technique. Results: In normal rats, NMDARl1 immunoreac-tivity positive structures couldbe seen in hippocampla CA1、 CA3 and dentate gyrus;1 h after KA injection, the density of NMDARi began to increase and got its maximun after 3h, then decreased gradually and after 24 h returned to the normal level. In the pre-stimulation group, the density of NMDAR1 in relevant brain regions decreased significantly. Conclusion: The antiepileptic function of VNS might be to reduce the NMDAR1 activity of neurons in vulnerable region.