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机构地区:[1]中山大学光华口腔医学院·附属口腔医院,广东省口腔医学重点实验室,广州510055 [2]广东省口腔医院·南方医科大学附属口腔医院正畸科
出 处:《中华口腔医学研究杂志(电子版)》2013年第3期31-35,共5页Chinese Journal of Stomatological Research(Electronic Edition)
基 金:国家自然科学基金(81170990);广东省科技计划(2011B090400097)
摘 要:目的研究正畸牙齿移动中前扣带皮质层(ACC)的蛋白激酶Mζ(PKMζ)表达变化,探讨中枢神经系统的突触可塑性是否参与了正畸牙齿移动中的疼痛形成。方法以250~300g的雄性Sprague-Dawley(SD)大鼠作为实验对象,观察术前1d,术后1、3、7d,大鼠挠嘴的平均时间。实验动物分别于术后1、3、7d处死,用免疫印迹方法研究ACC的PKMζ表达变化。结果研究发现,牙齿加力移动后1d(t18=-18.418,P<0.001)、3d(t18=-10.987,P<0.001)、7d(t20=-8.693,P<0.001),实验组大鼠的挠嘴行为明显多于对照组,差异具有统计学意义,在1d后达到高峰。免疫印迹的研究发现,牙齿加力移动1d(t18=-0.254,P>0.05)后,ACC的PKMζ的表达量与对照组无明显区别,加力3d(t18=2.636,P<0.05)后,PKMζ的含量明显增加,而7d(t20=0.939,P>0.05)后恢复到基础水平。结论 ACC中的PKMζ与牙齿移动引发的疼痛密切相关。突触可塑性可能参与牙齿移动过程中的疼痛机制。Objective Synaptic plasticity is a key mechanism for chronic pain. The aim of this study is to evaluate the expression of protein kinase M zeta (PKMζ) in the anterior cingulate cortex (ACC) after orthodontic force applied and to explore whether the synaptic plasticity is involved in the pain induced by experimental tooth movement. Methods Male Sprague-Dawley rats (250-300 g) were used in this study. A fixed, Ni-Ti alloy closed-coil spring appliance for mesial movement of the maxillary first molar was applied in rats of the experiment group. The average time spent on wiping mouth was measured on 1 day before, 1, 3, and 7 days after the surgery. Then, the animals were sacrificed for biochemical studies. The expression of PKMζ in the ACC was detected by western blot. Results Mouth- wiping behavior of rats was significantly increased on day 1 (t18=-18.418, P 〈 0.001), day 3 (t18=-10.987,P 〈 0.001) and day 7 (t20=-8.693, P 〈 0.001) after experimental tooth movement. However, the level of PKMζ was not changed on day 1 (t18=-0.254, P 〉 0.05), but increased on day 3 (t18= 2.636, P 〈 0.05) following the tooth movement. In addition, the levels of PKMζ returned to baseline on day 7 (t20=0.939, P 〉 0.05). Conclusion These results suggested that PKMζ was up-regulated in the anterior cingulate cortex and might act to maintain the pain induced by experimental tooth movement. Then, synaptic plasticity might be responsible for the pain caused by experimental tooth movement
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