全脑缺血-再灌注降低成年大鼠海马CA1区抑制性突触功能

Decreased inhibitory synaptic function in CA1 region of hippocampus of adult rats following global ischemia-reperfusion

目的观察全脑缺血-再灌注对成年大鼠海马CA1区抑制性突触功能的影响。方法成年雄性大鼠,随机分为:1)假手术组(SH)、2)缺血-再灌注3 d组(IR-3)、3)缺血-再灌注7 d组(IR-7)。用四动脉阻断法制作全脑缺血模型,使用全细胞电压钳技术记录海马脑片CA1区锥体细胞诱发的抑制性突触后电流(eIPSCs)。结果与SH组相比:低刺激强度时,IR-3及IR-7组eIPSCs的幅值明显降低(P<0.05);IR-7组eIPSCs的上升时间明显变短(P<0.05);IR-3组eIPSCs的配对抑制明显变大(P<0.05)。结论全脑缺血-再灌注降低了大鼠海马CA1区抑制性突触功能。

Objective To observe the effects of global ischemia-reperfusion on inhibitory synaptic function in hippocampal CAI region of adult rats. Methods Animals were randomly divided into three groups ： sham-operation group （SH）, ischemia-reperfusion 3 day （IR-3） and 7 day group （IR-7）. Global ischemic episode was achieved by 4-vessel occlusion. Evoked inhibitory postsynaptic currents （eIPSCs） were recorded from CA1 pyramidal cells in hippocampal slices using whole-cell voltage-clamp. Results The elPSCs amplitudes generated by lower stimulus intensities were significantly decreased in both IR-3 and IR-7 rats as compared with SH rats. Moreover, the rise time of elPSCs in IR-7 group was significantly decreased as compared with SH group （P 〈0. 05）,but the paired pulse depression elPSCs was significantly increased in IR-3 group as compared with SH rats. Conclusion Ischemia-reperfusion injury decreased GABA-mediated synaptic function in the hippocampal CA1 region of adult rats.