γ-氨基丁酸B受体亚单位R1b信使RNA在失神样癫痫发作时的改变  

GABA_B receptor subunit GBR1b pan mRNA in absence seizure model

作　　者：陆钦池[1] 苏敏[1] 蔡琰[1] 

机构地区：[1]上海第二医科大学附属仁济医院神经内科,200001

出　　处：《中华神经科杂志》2002年第6期351-353,共3页Chinese Journal of Neurology

摘　　要：目的　探讨γ 氨基丁酸B受体 (GABAB 受体 )亚单位R1b在失神样癫痫发病机制中的作用。方法　AY 9944大鼠癫痫模型是一种用胆固醇合成抑制剂连续腹腔内注射产生失神样癫痫发作的动物模型。用原位杂交法测定在失神样癫痫发作时GABAB 受体亚单位R1b(GBR1bpan)在鼠脑各部位的mRNA表达情况。结果　大脑皮层 海马及丘脑的mRNA表达均见不同程度的升高 ,以大脑皮层 [(361± 48)nCi/g]及海马CA1区域 [(32 7± 83)nCi/g]的改变最显著 (P值分别为 0 0 2和 0 0 2 7)。结论　GABABObjective To explore the possible mechanism of GABA B receptor subunit and epileptogenesis in absence seizure animal model Methods AY 9944 absence seizure model is developed by abdomenal injection of a cholesterol biosynthesis inhibitor Ay 9944 to neonatal Lon Evan hooded rats In situ hybridization is applied to detect GABA B receptor subunit GBR1b pan mRNA in rat brain of absence seizure Result There is increased hybridization signal in cortex, hippocampus and thalamus, especially in cortex (361±48 nCi/g) and hippocampus CA1 region (327±83 nCi/g)( P value 0 020 and 0 027 respectively) Conclusion The result of this study support the hypothesis that GABA B receptor subunit may be involved and induce seizures in absence epilepsy The finding of subunit change may direct the screen of new antiepileptic drug This finding deserves further study

关 键 词：γ-氨基丁酸B受体亚单位Rlb 信使RNA 失神样癫痫发作 发病机制 

分 类 号：R742.1[医药卫生—神经病学与精神病学]