AY-9944大鼠失神样痫性发作模型的GABA_B受体R1亚单位基因表达改变

目的 :探讨 GABAB受体亚单位在失神癫痫发病机制中的作用。方法 :用原位杂交的方法测定 AY- 9944大鼠癫痫模型在失神样痫性发作时 GABAB受体亚单位 GBR1a及 GBR1b pan m RNA在鼠脑的表达。结果 :大脑皮层 ,海马 CA1,CA3及丘脑的 GBR1a m RNA表达均见不同程度的升高 ,而以大脑皮层及海马 CA3区尤为显著。GBR1b pan大脑皮层 ,海马及丘脑的 m RNA表达均见不同程度的升高 ,而以大脑皮层及海马 CA1区域的改变最为显著。结论 :GABAB受体亚单位 GBR1可能参与失神性癫痫的发病机制 .这种受体亚单位的改变为筛选有效的抗癫痫药物提供新的途径。

GABAB receptor subunit GBR1 expression changes in AY-9944 absence seizure rat model

Objective: To expore the possible mechanism of GABA B receptor subunit and epileptogenesis in absence seizure rat model. Methods: AY-9944 absence seizure model is developed by abdomenal injection of a cholesterol biosythesis inhibitor Ay-9944 to neonatal Lon-Evan hooded rats. In situ hybridization is applied to detect GABA B receptor subunit GBRl a mRNA as well as GBRlb pan in rats brain ot absence seicure. Results: GBR1a mRNA expression levels are increased in cortex, hippocampus CA1and CA3 and thalamus, especially in cortex and hippocampus CA3 region. For GBR1b pan, there is increased hybridization signal in cortex, hippocampus and thalamus, especially in cortex and hippocampus CA1 region. Conclusion: The result of this study support the hypothesis that GABA B receptor subunit R1 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.