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作 者:崔占军[1,2] 赵凯冰[3] 邓洁心[1] 陈文静[1] 徐高磊[1] 邓锦波[1]
机构地区:[1]河南大学神经生物学研究所,河南开封475001 [2]河南大学医学院人体解剖学教研室,河南开封475001 [3]开封大学医学部解剖学教研室,河南开封475001
出 处:《解剖学报》2013年第5期594-601,共8页Acta Anatomica Sinica
基 金:国家自然科学基金资助项目(31070952;30771140;U1204311)
摘 要:目的探讨急性寒冷暴露对小鼠中枢神经系统的影响。方法选择生后40~50d的成年雄性小鼠40只,置于温度为0^-4℃环境中饲养20d,建立急性寒冷暴露模型。采用免疫细胞化学标记雌激素受体;DiI散射方法标记视皮质锥体细胞树突棘;利用透射电子显微镜观察突触的超微结构。结果急性寒冷暴露诱导小鼠视皮质锥体细胞树突棘的密度降低,形成的突触数量减少,部分突触出现树突胞质水肿、细胞器肿胀及微管减少等改变,明显抑制神经细胞增殖。结论急性寒冷暴露可导致神经系统的结构和功能改变,与雌激素及其受体G蛋白偶联受体30(GPR30)直接参与寒冷应激反应过程有关。Objective The objective of this study is to explore the effects of acute cold exposure to the mouse central nervous system. Methods To establish an acute cold exposure animal model, 40 adult male mice ofP40-50 were housed at 0℃ to -4℃ environment for 20 days. Estrogen receptors were labeled by immunohistochemistry; the dendritic spines of visual cortical pyramidal cells were labeled by DiI diolistic assay; and synaptic ultrastructure was observed by transmission electron microscopy. Results Acute cold exposure induced a decrease in the dendritic spine densities of mouse visual cortical pyramidal cells, along with a decrease in the number of synapse formations. The ultrastructures of some synapses were observed to have cytoplasmic and organellar swellings, as well as a decrease in microtubules. Furthermore, the proliferation of neural cells was significantly inhibited. Conclusion Acute cold exposure may cause structural and functional changes in the mouse central nervous system, possibly due to the direct participation of estrogen and its receptor, G protein-coupled receptor30 (GPR30), in acute cold response.
关 键 词:寒冷应激 树突棘 突触 视皮质 透射电子显微镜 DiI散射 小鼠
分 类 号:R749.6[医药卫生—神经病学与精神病学]
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