实验性脑梗死后突触体[Ca^(2+)]_i改变及神经生长因子治疗的影响

Changes of Intrasynaptosomal [Ca^(2+)]_1 in Cortex Periphery of Permanent Cerebral Infarction and Effect of Intraventricular injection of NGF

目的:探讨RHR脑梗死后病灶边缘额、顶叶皮层脑组织突触体内[Ca^(2+)]_i水平及其对神经生长因子(NGF)治疗的变化。方法:用Fura-2荧光标记,测定分离突触体内[Ca^(2+)]_i。结果:在RHR脑梗死后,静息状态下病灶边缘额、顶叶皮层脑组织突触体内[Ca^(2+)]_i在第3、7及14d明显升高,NGF脑室内注射12d后明显降低,同时减少运动障碍评分。结论:病灶边缘皮层突触体内[Ca^(2+)]_i的升高不利于神经运动功能的恢复,NGF降低突触体内[Ca^(2+)]_i促进运动功能恢复。

Aim: To investigate the mechanism of changes of cerebral cortex intrasynaptosomal free calcium concentration in penumbra of permanent cerebral infarction to motor functional recovery in renal vascular hypertensive rats(RHR) and the effect of intraventricular injection of nerve growth factor(NGF). Methods: The intrasynaptosomal [Ca2+]i was assayed by using Fura-2AM as fluorescent probe. Results: The intrasynaptosomal [Ca2+ ]i was increased about 2 times higher than control group within 3 days and remained in a relatively higher level until 30 days. Intraventricular injection of NGF could significantly decrease the elevated intrasynaptomal [Ca2+]i from 278. 13±47. 86 nmol to 236. 17±34. 71 nmol and also decreased the post-stroke neurological deficiency score. Conclusion: The intrasynaptosomal homeostasis plays a very important role in neuronal motor recovery after MCAO in RHR and the intraventricular injection of NGF could effectively decrease the elevated intrasynaptomal [Ca2+]i and promote the motor recovery.