慢性间歇性缺氧对海马齿状回神经再生的影响  

Effect of chronic intermittent hypoxia on neural regeneration in dentate gyrus

作　　者：唐婷[1] 黄延焱[1] 周厚广[1] 李祥云[1] 

机构地区：[1]复旦大学附属华山医院老年病科,上海200040

出　　处：《中国现代医学杂志》2011年第20期2333-2337,共5页China Journal of Modern Medicine

摘　　要：目的研究慢性间歇性缺氧对大鼠海马齿状回细胞增殖及突触形成的影响。方法建立SD大鼠慢性间歇性缺氧模型,检测海马齿状回细胞增殖、突触素表达、乙酰胆碱M 1受体及N-甲基-D-天门冬氨酸受体1(N R 1)水平。结果与正常对照组相比,慢性间歇性缺氧模型大鼠海马齿状回BrdU光密度值(O D值)、突触素O D值、乙酰胆碱M 1受体O D值及N-甲基-D-天门冬氨酸受体1O D值均显著增高(均P<0.05)。结论慢性间歇性缺氧诱导了海马齿状回的细胞增殖,同时使突触素、乙酰胆碱M 1受体和N-甲基-D-天门冬氨酸受体1表达增加,可能与缺氧诱导的海马齿状回神经细胞代偿性增加有关。【Objective】 To investigate the characteristics of cell proliferation and synaptogenesis in the dentate gyrus after chronic intermittent hypoxia.【Methods】 SD rats were exposed to intermittent hypoxia for 8 weeks to establish chronic intermittent hypoxia model of rat.The expression of BrdU,synaptophysin,CHRM1（Muscarinic Acetylcholine Receptor M1） and NR1（N-methyl-D-aspartate Receptor 1） were tested in the rats＇ dentate gyrus.【Results】 Compared with the normal control group,rats with chronic intermittent hypoxia showed increased optical density of BrdU＋,synaptophysin,CHRM1 and NR1 in dentate gyrus（P 0.05）.【Conclusion】 The dentate gyrus undergoes specific changes after chronic intermittent hypoxia,including cell proliferation and the expression of synaptophysin,CHRM1 and probably the result of hypoxia induced neural regeneration in dentate gyrus.

关 键 词：海马齿状回 慢性间歇性缺氧 神经再生 突触素 乙酰胆碱M1受体 N-甲基-D-天门冬氨酸受体1 

分 类 号：R-332[医药卫生]