丝切蛋白棒状结构致慢性脑低灌注大鼠海马突触丢失

Cofilin rod leads to synaptic loss in hippocampus of rats with chronic cerebral hypoperfusion

目的观察丝切蛋白棒状结构在慢性脑低灌注大鼠海马区的表达,探讨其在慢性脑低灌注大鼠突触可塑性中的作用。方法运用随机数字表法将25只SD健康成年雄性大鼠分成慢性脑低灌注组(15只)和假手术组(10只)。双侧颈总动脉永久性结扎方法制备慢性脑低灌注模型组。假手术组方法同前,但是只分离双侧颈总动脉而不结扎。两组大鼠于造模后第4周做水迷宫测试。水迷宫测试完后第2天处死大鼠并取其海马组织制成冰冻切片。运用免疫荧光双重标记大鼠海马区丝切蛋白和突触素。结果慢性低灌注组大鼠学习记忆能力较假手术组明显受损(P<0.05)。慢性低灌注组大鼠海马区丝切蛋白棒状结构形成。慢性低灌注组突触素较假手术组显著减少(P<0.05)。结论慢性脑低灌注大鼠海马丝切蛋白棒状结构导致突触丢失,这可能是慢性脑低灌注所致学习记忆受损的主要因素。

Objectives To observe the expressions of cofilin-actin rods in hippocampus of rats suffering from chronic cerebral hypoperfusion. Methods By using the method of random number table, 25 healthy male S-D rats were divided into chronic cerebral hypoperfusion group and sham operation group. Chronic cerebral hypoperfusion model group was prepared by permanent ligation of bilateral common carotid arteries. The sham operation group with the former method, but only separated the bilateral common carotid artery without ligation. Morris water maze was used to assess the spatial learning and memory abilities, and the expressions of cofilin-actin rod and synaptophysion in hippocampus were estimated by double immunofluorescent labeling method. Results The abilities of spatial learning and memory in chronic cerebral hypoperfusion groups were significantly decreased, and the expressions of synaptophysion in hippocampus were also degraded compared with the sham operation group. Importantly, cofilin-actin rod formation induced a significant loss of synaptophysin puneta. Conclusion Cofilin-aetin rod may contribute to synaptic loss and were associated with the cognitive impairment induced by chronic cerebral hypoperfusion in rats.