摘要
目的探讨氯胺酮不同暴露时间下对发育神经元肌细胞增强因子2(MEF2)信号通路及突触生长相关蛋白synapsin I表达影响。方法新生5 d龄SD大鼠,随机分为2,4,6和24 h氯胺酮组(T组)和对照组(C组)。将新生5d SD大鼠皮下注射氯胺酮(20 mg·kg-1)干预。对照组不做任何处理。干预后在各对应时间点提取海马神经元总RNA,利用real-time PCR进行定量分析MEF2信号通路(MEF2 mRNA、synGAP I mRNA和Arc mRNA)及突触形成相关基因synapsin I mRNA表达水平。结果与C组相比,用氯胺酮干预后时间依赖性下调海马神经元MEF2 mRNA、synGAP I mRNA、Arc mRNA(P<0.05)。Synapsin I mRNA表达则时间依赖性上调(P<0.05)。麻醉后24 h恢复正常。结论氯胺酮短暂下调MEF2信号通路而上调synapsin I表达,其机制可能是Arc表达上调增加突触数目以致synapsin I表达上调。
Objective To investigate the time-dependent effects of ketamine on myocyte enhancer factor 2（ MEF2）signaling pathway and expression of synaptogenesis synapsin I of rat developing hippocampal neurons in vivo. Methods Forty5-day-old rats were randomly divided into 4 treatment groups receiving ketamine （20 mg·kg-1 ） single injection and a controlgroup receiving no treatment. Pups were killed by decapitation to extract total RNA from hippocampal neurons in the 4 treatmentgroups at 2, 4, 6,24 h, respectively, and from the control group. Real-time-PCR was used to detect the expression of the MEF2mRNA、synGAP I mRNA and Arc mRNA and synapsin I mRNA after intervention. Results Compared with the control group,there are significant decreases in the expression of MEF2 mRNA, synGAP I mRNA, Arc mRNA and increase in synapsin ImRNA of the neurons from ketamine treatment groups（P〈0. 05）. Conclusion The mechanism of ketamine-induced decreasein expression of MEF2 signaling pathway and increase in the expression of synapsin I may be related to decreased expression ofArc signaling pathway, which in turn regulates the expression of snapsin I in the developing hippocampal neurons
出处
《医药导报》
CAS
北大核心
2014年第4期419-421,共3页
Herald of Medicine
基金
国家自然科学基金资助项目(81200880)
