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目的:观察短时脑缺血再灌后大鼠海马CA1神经元自发放电活动的改变以及地昔帕明(Des)对其放电频率的影响。方法:短暂性脑缺血(10min,4-VO法)3d后,细胞外记录CA1神经元单位放电的变化,尾静脉给药。实验结束后对海马切片进行形态计量检查。结果:再灌d 3海马CA1细胞放电活动明显增加。Des(0.2&0.4 mg·kg~(-1),iv)能显著减弱CA1区升高的放电频率,其最大抑制率分别在给药后6min(58％&85％)至9min(69％&94％)期间,与生理盐水对照值相比差异显著(ANOVA,P<0.01)。组织学显示该区约50％锥体细胞呈缺血坏死。结论:Des能颉抗海马缺血后的高兴奋性活动。
Objective: To observe the changes of spontaneous discharge activity of hippocampal CA1 neurons in rats after transient focal cerebral ischemia and reperfusion, and the effect of desipramine on the discharge frequency. Methods: The changes of unit discharge of CA1 neurons were recorded extracellularly after transient ischemic (10 min, 4-VO) for 3 days. The hippocampal slices were morphologically examined after the experiment. Results: The discharge activity of hippocampal CA1 cells was significantly increased after reperfusion. Des (0.2 and 0.4 mg · kg -1, iv) significantly attenuated the increase of discharge frequency in CA1 region, and the maximum inhibitory rate was 6 min (58% & 85%) to 9 min %), There was significant difference compared with saline control (ANOVA, P <0.01). Histology showed that about 50% pyramidal cells in this area showed ischemic necrosis. Conclusion: Des can antagonize hippocampus hyperactivity activity after ischemia.