| Summary: | 碩士 === 國立嘉義大學 === 生化科技學系研究所 === 96 === Neurogenesis, the process of newly generated neurons, occurs mainly in the subventricular zone (SVZ) and the subgranular zone (SGZ) of the dentate gyrus (DG). Various physiological stimuli could modulate neurogenesis in these regions which include glucocorticoid, estrogen, growth factors, excitatory neurotransmission, learning and stress can be manipulated pharmacologically. It is also evidenced that pathological events can stimulate adult neurogenesis such as seizures, ischemia, traumatic brain injury and subarachnoid hemorrhage (SAH). SAH is a life-threatening disorder of the central nervous system with high mortality and morbidity rates mainly associated with primary brain damage and cerebral vasospasm. Previous results showed vascular endothelial growth factor (VEGF) could stimulate neuronal precursors and promotes neurogenesis. Our previous study demonstrated that VEGF is necessary for traumatic brain injury-induced neurogenesis. The present study aimed to evaluate the effect of VEGF on neurogenesis after SAH. We used double hemorrhage model of SAH by injection of autologous blood twice into cisterna magna of rats. Rats received intraperitoneal injections of 5’-bromo-2’-deoxyuridine (BrdU) after SAH induction. The expression of VEGF was detected by RT-PCR and Western blot. Immunofluorescence double labeling was used to evaluate the distribution of BrdU, doublecortin (DCX) and VEGF. In this study, we found that expression of VEGF mRNA and protein significantly increased in cortex and hippocampus seven days after SAH. We also found that the hippocampal neurogenesis was decreased at day 3 after SAH, and was backed to the normal level at day 9. Administration of VEGF antisense oligonucleotides significantly attenuated SAH-induced neurogenesis. Our study demonstrated that VEGF plays an essential role in hippocampal neurogenesis after SAH.
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