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作 者:贾一凡[1] 韩永慧[1] 陶媛媛[1] 王贞贞[1] 李子墨 赵健[2] JIA Yifan HAN Yonghui TAO Yuanyuan et al(Department of Clinical Medicine ,Class of 2013, Wannan Medical College ,Wuhu City ,Anhui Province 241002)
机构地区:[1]皖南医学院临床医学院,安徽省芜湖市241002 [2]皖南医学院人体解剖学教研室,安徽省芜湖市241002
出 处:《医学理论与实践》2016年第19期3301-3303,共3页The Journal of Medical Theory and Practice
基 金:安徽省大学生创新训练项目(AH201410368134)
摘 要:目的:探讨短期睡眠剥夺对幼年大鼠海马CA1区生长抑素和β1-肾上腺素受体表达的影响。方法:将40只雄性幼年大鼠随机分为对照组、12h、24h、36h和48h睡眠剥夺组,每组8只。采用改良多平台水环境法建立大鼠SD模型,免疫组织化学法检测海马CA1区SS、β1-AR的表达量。结果:12h、24h、36h睡眠剥夺组大鼠海马CA1区SS阳性神经元的数量较对照组均显著增多(P<0.01),48h睡眠剥夺组大鼠海马CA1区SS阳性神经元的数量较对照组明显减少(P<0.01);12h、24h、36h睡眠剥夺组大鼠海马CA1区β1-AR阳性神经元的数量较对照组均显著增多(P<0.01),48h睡眠剥夺组大鼠海马CA1区β1-AR阳性神经元的数量较12h、24h、36h睡眠剥夺组明显减少,但仍高于对照组(P<0.01)。结论:睡眠剥夺36h内幼鼠海马CA1区神经元SS、β1-AR的表达量增加,可能参与代偿性神经保护机制,而48h后SS、β1-AR的表达量显著下降,提示海马CA1区神经元可能已受损,致学习记忆障碍。Objective:To observation the impact of short-term sleep deprivation on somatostatin andβ1-adrenoceptor expression in hippocampal CA1 area in young rats.Methods:40young male rats were randomly divided into the control group,12 hSD group,24 hSD group,36 hSD group,48 hSD group,8rats in each group.Methods SD was induced in male rats by using modified multiple platform method,then detect the expression of somatostatin andβ1-adrenoceptor in hippocampal CA1 area by immunohistochemical method.Results:The number of SS positive neurons in hippocampus CA1 area of 12 h,24hand 36 hsleep deprivation group were significantly increased compared with the control group(P〈0.01),while 48 hsleep deprivation group was significantly lower than that in control group(P〈0.01).The number ofβ1-adrenoceptor positive neurons in hippocampus CA1 area of 12 h,24hand 36 hsleep deprivation group were significantly increased compared with the control group(P〈0.01),48 hsleep deprivation group was significantly lower than that in 12 h,24h,36 hgroup,but still higher than that in control group(P〈0.01).Conclusion:SS andβ1-AR positive neurons of neurons in hippocampal CA1 area of sleep deprivation increased within 36 hmay in compensatory neuroprotective mechanism,while the expression was significantly reduced after 48 h,suggest that neurons of the hippocampal CA1 area may have been damaged,resulting in impairment of learning and memory.
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