全脑缺血-再灌注对海马CA1区GAD65表达的影响及意义

Effect and significance of global ischemia-reperfusion on the expression of GAD65 in hippocampal CA1 region

目的探讨全脑缺血-再灌注对成年大鼠海马CA1区GAD65表达的影响及意义。方法成年雄性SD大鼠24只,随机分为3组:假手术组(SH)、缺血-再灌注3d组(IR-3)及缺血-再灌注7d组(IR-7),每组8只。采用四动脉阻断法制作全脑缺血-再灌注模型,应用免疫组织化学方法检测海马CA1区谷氨酸脱羧酶(glutamic acid decarboxylase,GAD)同工酶GAD65的表达变化。结果与假手术组相比,IR-3组GAD65的表达明显增多,IR-7组恢复正常。结论GABA能中间神经元对缺血相对耐受;全脑缺血-再灌注3dGAD65的表达增多可能是一种代偿性的机制,以减轻脑缺血后的高兴奋性。

Objective To observe the effect of global ischemia-reperfusion on the expression of GAD65 in the hippocampal CA1 region of adult rats. Methods 24 male SD rats were randomly divided into three groups： sham-operation group （SH,n=8）, ischcmia-reperfusion three days （IR-3 ,n= 8） and seven days group （IR-7, n = 8）. Global ischemic episode was achieved by 4-vessel occlusion. Immunohistochemical method was applied to observe the expression of GAD65 in hippocampal CA1 region. Results At ischemiareperfusion third day, the immunoreactivities of the GAD 65 were markedly elevated in the CA1 region compared with sham operated group, but the immunoreactivities recovered to the sham level at ischemia-reperfusion seventh day. Conclusion GABAergic interneurons relatively resistant to ischemia-reperfusion injury, and the increasing expression of GAD65 3d after ischemia-reperfusion can be a compensatory mechanism to reduce the hyperexcitability associated with ischemia-reperfusion.