中文摘要：

目的探讨阻断缝隙连接对大鼠局灶性脑缺血后海马迟发性神经元死亡（DND）及神经行为学的影响。方法术前2h左侧脑室注射缝隙连接阻断剂甘珀酸（CBX），对照组左侧脑室注射生理盐水，颈内动脉插线法制备大鼠大脑中动脉缺血-再灌注模型。术后72h采用尼氏染色检测海马迟发性神经元死亡，术后24h和72h进行神经行为学评分．数据进行统计学分析，观察阻断缝隙连接对大鼠局灶性脑缺血72h后海马迟发性神经元死亡及神经行为学的影响。结果不用CBX预处理，大脑中动脉缺血模型72h后有45％的动物出现海马DND，用CBX预处理后．DND发生率降到30％．较对照组明显降低（P〈0．01）。CBX干预组的行为学评分明显比对照组低（P〈0．01）。结论阻断缝隙连接可以减少局灶性脑缺血后海马迟发件神经元死亡的发生率，改善局灶性脑缺血术后动物行为学表现。

英文摘要：

Objective To explore the effect of blocking gap junction communication after focal cerebral ischemia on delayed neuronal death in ipsilateral hippocampus and the neurological scores. Methods A rat model of middle cerebral artery occlusion （MCAO） was made by the intraluminal occlusion teehnique. Carbenoxolone, a gap junction blocker, was used to block gap junction communication, and the effect of blocking gap junction communication after focal cerebral ischemia on delayed neuronal death in the ipsilateral hippocampus was observed by Nissl＇s staining and the neurological scores were evaluated in all rats in 24 h and 3 days after operation. Results With no inhibition of gap junction communication, delayed neuronal death was detected in 45% of the animals in hippocampal CAI region 3 days after middle cerebral artery occlusion. With the inhibition of gap junction communication, delayed neuronal death appeared in only 30% of the animals, which was significantly lower than that of control group （P〈0.01）. Meanwhile, compared with those in control group, the neurological scores of the animals in experimental group were significantly reduced （P〈0.01）. Conclusion Blocking gap junction communication can reduce the incidence of delayed neuronal death in hippocampus after MCAO, and can prevent neurological deficiency after MCAO.