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探讨脑缺血再灌流不同时程及不同程度缺血对海马及皮层胶质源性神经营养因子(glialcellline derived neurotrophic factor, GDNF)基因表达的影响,以及N甲基D天冬氨酸(Nm ethylDsapartate, NMDA)受体拮抗剂,钙离子通道阻断剂是否能调节缺血病态下GDNFm RNA的表达。参照Sm ith 等方法建立大鼠前脑缺血再灌流动物模型。用DIGOligonucleotide 3′end labeling Kit,标记51 m er的GDNF寡核苷酸探针在含有海马结构的冰冻组织切片上进行原位杂交检测GDNFm RNA的表达。10 m in 缺血再灌流2 h,齿状回GDNFm RNA表达上调。再灌流6 h,CA1,CA3 和皮层PAR区GDNFm RNA表达亦见增多,24 h 达高峰。Ketam ine 可使GDNF的基因表达在海马结构及皮层PAR区明显低于相应的缺血再灌流组,统计学差异显著(P< 005)。脑缺血再灌流时GDNF基因表达增加,对缺血神经元可能起保护作用。Ketam ine可阻断缺血后GDNFm RNA 的表达增加,提示NMDA谷氨酸受体很可能参与介导了缺
To investigate the effect of ischemia and reperfusion at different time points and different degrees of ischemia on gene expression of glial cell line derived neurotrophic factor (GDNF), and Nmethyl D aspartate NMDA receptor antagonist and calcium channel blocker could regulate the expression of GDNFm RNA in ischemic condition. According to Smith and other methods to establish forebrain ischemia reperfusion animal model in rats. GDNFm RNA expression was detected by in situ hybridization on frozen tissue sections with hippocampal formation using the GIGF oligonucleotide probe labeled with 51 m er of DIG-Oligonucleotide 3’-end labeling kit. The expression of GDNFm RNA in the dentate gyrus was up-regulated at 10 min after ischemia-reperfusion. At 6 h after reperfusion, the expression of GDNFm RNA also increased in CA1, CA3 and cortical PAR regions, reaching the peak at 24 h. Ketamine gene expression of GDNF in the hippocampal structure and cortical PAR area was significantly lower than the corresponding ischemic reperfusion group, a statistically significant difference (P <0 05). GDNF gene expression increases after cerebral ischemia and reperfusion and may play a protective role on ischemic neurons. Ketamine can block the increase in GDNFm RNA expression after ischemia, suggesting that NMDA-glutamate receptors are likely to be involved in the mediation of the lack of