IL-1β对谷氨酸致痫大鼠大脑皮质、海马内NMDAR_1免疫反应变化的影响

为了进一步探讨 IL -1β在促进癫痫发作中的机制 ,用免疫组织化学方法比较了单纯用致痫量谷氨酸钠致痫的大鼠和预先向侧脑室注射 IL-1β再用阈下剂量的谷氨酸钠共同致痫的大鼠脑内 NMDAR1 免疫反应的变化。结果表明 ,IL-1β和谷氨酸钠共同致痫的大鼠大脑皮质及海马 CA3区 NMDAR1 免疫反应较对照组明显增强 (P<0 .0 5 ) ,与单纯用谷氨酸钠致痫的大鼠没有明显区别。如果预先给予 IL-1ra或 D-AP5则 IL-1β和谷氨酸钠的共同致痫效果不出现 ,脑内 NMDAR1 免疫反应与对照组比较未见明显增强 (P>0 .0 5 )。本实验结果表明 ,IL -1β具有促进癫痫发作的效应 ,这种促癫痫效应的发挥与谷氨酸受体具有协同作用 ,并与通道型 NMDA受体 R1 亚单位表达的增加有关

EFFECTS OF IL-1β ON THE VARIATION OF NMDA RECEPTOR SUBUNIT 1 IMMUOREACTION IN RATS WITH SEIZURE INDUCED BY L-GLUTAMATE

We explored the mechanism of IL 1β in the onset of seizure. Experimental rats were injected with IL 1β first and then L glutamate (a dose under the threshold) into the lateral ventricle and were sacrificed 2 hours after the onset of epileptic activity. The changes of NMDAR 1 were examined by means of immunohistochemistry and compared with that of rats with seizure induced by L glutamate alone. We found that the immunoreaction of NMDA receptor subunit 1 in hippocampal CA 3 area and neocortex of rats with seizure induced by IL 1β and L glutamate were greater than that of control group(P<0.05).Whereas there were no remarkable differences in the immunoreaction of NMDAR 1 between the two experimental group of rats. Pre application of IL 1ra or D AP5, eliminated the epileptic activities and the increased immunoreaction of NMDAR 1 induced by IL 1β and L glutamate. The expression level of NMDAR 1, under this conditions was no difference with that of control rats. These results indicate that IL 1β can facilitate the onset of epilepsy by L glutamate through the cooperation between IL 1R and glutamate receptors, and that the increased expression of NMDAR 1 is involved in the process.