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作 者:喻志源[1] 李杰[1] 刘仁刚[2] 王伟[1] 骆翔[1]
机构地区:[1]华中科技大学同济医学院附属同济医院神经内科,武汉430030 [2]华中科技大学同济医学院人体解剖学系,武汉430000
出 处:《解剖学报》2010年第6期790-795,共6页Acta Anatomica Sinica
基 金:国家自然科学基金资助项目(30800341);国家杰出青年基金资助项目(30725019)
摘 要:目的研究大鼠大脑中动脉缺血再灌注后,梗死对侧皮层氨基丁酸A(GABAA)受体α2和α3亚基的表达变化。方法采用大鼠大脑中动脉阻塞(MCAO)再灌注模型,分为MCAO组(n=18)和假手术组(n=18),分别于术后7d、30d和6个月断头取脑,采用免疫组织化学技术检测各组中梗死对侧皮层GABAA受体亚基α2和α3的表达情况。结果 MCAO组大鼠与假手术组大鼠相比,在7d时梗死对侧亚基α2和α3在皮层各个脑区改变无明显差异(P>0.05);30d和6个月时,亚基α3在各个脑区均显著升高(P<0.05);30d时亚基α2在梗死对侧的Par1和Par2脑区表达增加(P<0.05);6个月时,梗死对侧亚基α2在Par1脑区表达增加而在Par2脑区表达降低(P<0.05)。结论大鼠大脑中动脉缺血再灌注后梗死塞对侧皮层GABAA受体亚基α2和α3发生了广泛而长效的变化,这种变化提示脑缺血后GABAA受体功能受损,GABAA受体的改变可能参与了缺血后突触的重塑和神经网络重建。Objective To study the expressions of GABAAreceptor subunits α2 and α3 after middle cerebral artery occlusion/reperfusion in rats. Methods The animals in the experimental groups were subjected to transient middle cerebral artery occlusion (MCAO) using the intraluminal thread model. The rats were randomly distributed into MCAO group (n = 18)and sham group( n = 18). Rats were sacrificed at the 7th day, 30th day and 6th month after operation. Immunohistochemical staining was used to detect the expressions of GABAA receptor subunits α2 and α3 between MCAO and sham group. Data were analyzed by SPSS software. Results In the contraiateral cortex, there were no significant difference of subunits α2 and α3 expression between MCAO group and sham group in 7 days after ischemia. In 30 days and 6 months, the expression of subunit α3 in H1,Fr,Parl and Par2 brain regions was markedly higher than that of sham group in eontralateral cortex (P 〈 0.05). In 30 days, the expression of subunit α2 in MCAO group was higher than that of sham group in Parl and Par2 brain regions (P 〈 0. 05) ; however, in 6 months the expression of subunit α2 was lower in Par2 and higher in Parl compared with sham group (P 〈 0.05). Conclusion The expressions of subunits α2 and α3 have a generalized and long-term change after middle cerebral artery ischemia /reperfusion in rats' contralateral cortex. These findings suggest that the function of GABAA receptor is impaired and these changes may be involved in the remodeling of synapses and neural network reconstruction after focal brain isehemia.
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