地昔帕明对大鼠短暂脑缺血致海马CA1神经元自发放电的影响(英文)

Effect of desipramine on spontaneous activity of hippocampal CA1 neuron after transient cerebral ischemia in rats

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。

AIM: To study the spontaneous firing of CA1 neurons in rat hippocampus after transient cerebral ischemia and the effect of desipramine (Des) on the post-ischemic electric activity of CAl neurons. METHODS: Single-unit extracellular recordings were performed in rats on d 3 after 10 min of cerebral ischemia by occlusion of 4 arteries. Des and saline were injected into a tail vein. The histological changes of CAl neurons was assessed by the neuronal density of the CAl sector. RESULTS: The spontaneous firing rate of CAl neurons on d 3 after ischemia was enhanced in comparison with the control value. Des (0. 2 and 0.4 mg @ kg-1, iv, n=5 & 6, respectively) reduced dose-dependently the increase of firing rate with maximal inhibition by 6 min (58 % &. 85 %) to 9 min (69 % & 94 %) (vs vehicle group, P<0. 01). About 50 % cells in CAl region showed necrotic changes. CONCLUSION: Des antagonized the hyperexcitability of CAl neurons after cerebral ischemia.