TBOA抑制谷氨酸转运体功能对戊四氮点燃癫痫模型的影响

Effect of glutamate transporter inhibitor TBOA on epilepsy induced by pentylenetetrazol in rats

目的:研究新型谷氨酸转运体抑制剂TBOA对戊四氮点燃癫痫的发生及神经病理作用,寻找治疗戊四氮点燃癫痫的新方法。方法:戊四氮慢性点燃方法进行造模,分为癫痫组和TBOA治疗组。TBOA治疗组造模前3d大鼠侧脑室注射TBOA,癫痫组侧脑室注射生理盐水。2周后处死大鼠,研究两组癫痫的发生率、海马及皮质的病理改变、神经元计数。结果:1d的癫痫发生率在癫痫组为87.5%,TBOA治疗组为40.6%,光镜显示TBOA治疗组的损害程度轻于癫痫组。1、3d时海马CA1区神经元计数癫痫组与TBOA治疗组比较差异有显著性(P<0.01);5、7d时,癫痫组神经元计数少于TBOA治疗组(均P<0.05)。皮质区变化规律同海马CA1区。结论:早期应用谷氨酸转运体抑制剂TBOA能降低癫痫的发生率,并改善癫痫后神经病理损害。

Objective To study the effect of new type glutamate inhibitor TBOA on the occurrence of epilepsy induced by pentylenetetrazol （PTZ） in rats. Methods The reliable rat models with epilepsy kindled by PTZ were assigned to receive injection of TBOA （TBOA group） or injection of normal saline （epilepsy group） into lateral ventricle 3 days before PTZ assignment. The incidence of epilepsy, the pathological changes of hippocampus and cortex, and the neuron count were measured. Results The incidence of epilepsy in epilepsy group and TBOA group were 87.5% and 40.6%. The optical microscope showed that the injury in TBOA group was slighter than that in epilepsy group. As for the neuron count in CA1 area, there was a significant difference between the two groups at the early stage （ 1 d and 3 d） （P 〈 0.01 ） ; the neuron count in epilepsy group was less than that in TBOA group at the later stage （5 d and 7 d）（P 〈 0.05）. The changes of neuron count in the cortex area was similar. Conclusion Application of glutamate transporter inhibitor TBOA before PTZ treatment can decrease the incidence of epilepsy and alleviate neuropathological damage after epilepsy.