摘要
目的观察新型的谷氨酸转运体抑制剂 TBOA 对全脑缺血性癫癎的发生及神经病理的作用,探索全脑缺血性癫癎的治疗新方法。方法应用稳定可靠的大鼠胸部压迫8min 全脑缺血性癫癎模型,分为缺血癫癎组和 TBOA 治疗组。胸部挤压前3d大鼠侧脑室内注射 TBOA,研究两组癫癎的发生率、海马及皮质病理改变、神经元计数。结果缺血后24h 癫癎发生率在缺血癫癎组为61%,TBOA 治疗组为40%,光镜病理显示,TBOA 治疗组损害程度轻于缺血癫癎组。海马 CAI 区神经元计数:缺血早期(24h,72h 组),缺血癫癎组与 TBOA 治疗组比较无显著性差异,P>0.05;缺血后期(5d,7d 组),缺血癫癎组神经元计数少于TBOA 治疗组,P 均<0.05。皮质区变化规律同海马 CAI 区。结论全脑缺血前应用谷氨酸转运体抑制剂 TBOA 能降低癫癎的发生率,并改善缺血后神经病理损害。
Objective To observe the occurrence of epilepsy relative to global cerebral ischemia and neuropatho- logic effect by using newtype glutamate transporter inhibitor TBOA and to explore the new method for treatment of epi- lepsy relative to global cerebral ischemia.Methods The reliable rat models with global cerebral ischemia by chest compression for 8 min were established.They were divided into the ischemic epilepsy group and the TBOA treatment group.Before chest compression,TBOA was injected into the anteriolateral ventricle of the brain to study the inci- dence rate of epilepsy,pathologic changes of hippocampus and cortex,and neuron count between the two groups. Results After ischemia 24 h the incidence rate of epilepsy in the ischemic epilepsy group amounted to 61% and that in the TBOA treatment group accounted for 40%.The optical microscope showed that the injury in the TBOA treat- ment group was slighter than that in the ischemic epilepsy group.As for the neuron count in CAI area,there was no marked difference between the ischemic epilepsy group and the TBOA group at the early ischemic stage(24 h,72 h) (P>0.05);the neuron count in the ischemic epilepsy group was less than that in the TBOA group at the later ische- mic stage(5 d,7 d)(P<0.05).The changes in the cortex area was similar to that in CAI area of hippocampus. Conclusion Using glutamate transporter inhibitor TBOA before global cerebral ischemia can decrease the incidence rate of epilepsy and alleviate neuropathological damage after ischemia.
出处
《神经病学与神经康复学杂志》
2006年第3期163-165,共3页
Journal of Neurology and Neurorehabilitation
关键词
谷氨酸转运体
TBOA
全脑缺血
癫癎
glutamate transporter inhibitor
TBOA
global cerebral ischemia
epilepsy