脑性瘫痪幼鼠脑谷氨酸脱羧酶、γ-氨基丁酸A受体表达的变化

Effcets of the glutamic acid decarboxylase and gamma- aminobutyric a cid receptor A in cerebral palsy

目的:观察缺氧缺血窒息脑性瘫痪(简称脑瘫)幼鼠脑中谷氨酸脱羧酶(GAD),氨基丁酸A受体(GABAA)α1,β2两种亚单位受体表达的变化,探讨GAD,GABAAα1,β2在脑瘫中的作用机制。方法:采用改良的Philip方法,建立缺氧缺血窒息脑瘫模型;应用免疫组织化学ABC方法,检测缺氧缺血后不同时间大脑、海马中GAD,GABAA受体α1,β2亚单位表达的变化情况。结果:单位面积(mm2)大脑皮质中GAD阳性细胞数在缺氧缺血后2h增高48%,24h接近正常,海马中变化不明显;1mm2皮层及海马中GABAA受体α1mRNA阳性细胞数在缺氧缺血后12h下降分别达49%和60%,96h最为显著,分别达66%和70%;而大脑皮质和海马中β2亚单位1mm2阳性细胞数在2h下降分别达41%和38%,48h下降最为明显均为57%。结论:缺氧缺血初期脑瘫鼠脑中GAD的增加是机体的一种自我保护机制;GABAA受体α1,β2亚单位的减少,使GABA作用于GABAA受体所产生的突触后抑制效应降低,参与了脑瘫的形成。

AIM: To observe the change of the expression of the glutamic acid decarboxyla se( GAD) and gamma- aminobutyric acid( GABAA) receptorá 1,a 2 in the bra in of the cerebral palsy postnatal rat after hypoxic- ischemic and to explore t heir mechanisms in the cerebral palsy(CP). METHODS:An improved Philips methods was used and a model of cerebral palsy w as created.An immunohistochemistry method was used to detect the change of the e xpression of the GAD and GABAA receptor á 1,a 2 subunits in the brain after hy poxic- ischemic at different times. RESULTS:The count of unit surface area( mm2) positive cells mRNA of the GAD was significantly increased by 48% in the cerebral cortex at 2 hours and was back to normal at 24 hours after hypoxic- ischemic, however, there was no signi ficant changes in the hippocampus. That of the the GABAA receptor á 1 subunit b egan to decrease 49% and 60% at 12 hours,and obviously decreased 66% and 7 0% at 96 hours in the cerebral cortex and hippocampus respectively after hypox ic- ischemic, that of thea 2 subunit decreased 41% and 38% at 2 hours resp ectively and reduced 57% at 48 hours in both position. CONCLUSION:In the initial stage of the hypoxic- ischemic,the increase of GAD may be a self- protective mechanism;the effect of postsynaptic inhibition of G ABA acting on GABAA reduce cause of the decrease of GABAA receptor á 1,a 2 su bunit receptor, and may be associated with the process of cerebral palsy.