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作 者:艾卫敏[1,2] 左剑斌[1,3] 朱耀峰[1,4] 周奕[1,5] 雷德亮[1] 李昌琪[1] 邓小华[1]
机构地区:[1]中南大学湘雅医学院人体解剖学与神经生物学系,长沙410013 [2]湘潭职业技术学院护理学院人体解剖学与生理学教研室,湘潭411012 [3]湘潭职业技术学院医学技术学院免疫学教研室,湘潭411012 [4]吉首大学医学院解剖学教研室,吉首416000 [5]长沙卫生职业学院基础学部解剖与组织胚胎学教研室,长沙410100
出 处:《神经解剖学杂志》2012年第4期347-351,共5页Chinese Journal of Neuroanatomy
基 金:湖南省自然科学基金项目(07JJ5047);湖南省科技厅科研课题项目(2011FJ4166);湖南省教育厅科学研究项目(10C0304)
摘 要:目的:探讨海马内注射LPS(lipopolysaccharide,LPS)后,大鼠皮质神经元和星形胶质细胞PirB(paired-immunoglobulin-like receptor B)的表达变化。方法:成年SD大鼠,分为对照组和实验组,用免疫组织化学法检测大鼠脑皮质PirB的表达及星形胶质细胞GFAP的表达变化,免疫荧光双重标记技术,观察星形胶质细胞与PirB阳性细胞的共存。结果:PBS注射的对照组动物脑皮质Ⅴ层内可见PirB阳性神经元样细胞,呈圆形、卵圆形和锥体形,免疫反应产物呈棕色、主要位于细胞膜上;海马内注射LPS 30 d后,PirB阳性神经元样细胞和PirB阳性神经胶质样细胞主要分布于皮质Ⅳ、Ⅴ层,免疫反应产物位于胞质和突起内;另外,可见大鼠梨状皮质、内嗅皮质内GFAP阳性星形胶质细胞明显被激活,表现为细胞胞体相对增大,突起变粗。PirB分别和MAP-2、GFAP、CD11b免疫荧光双重标记染色显示:PirB和MAP-2阳性神经元的胞体存在共定位;PirB与GFAP阳性染色存在部分共定位,但未见PirB与CD11b阳性染色双标细胞。结论:LPS能诱导大鼠皮质星形胶质细胞活化和PirB蛋白表达上调,而且部分活化的星形胶质细胞表达PirB,PirB可能参与脑内炎症突触可塑性改变和学习记忆功能缺失的免疫调节。Objective: To investigate the changes of the paired-immunoglobulin-like receptor B (PirB) expression in neurons and glial cells in rat cortex after a single intrahippocampal (ih) injection of lipopolysaccharide (LPS). Meth- ods:SD rats were divided into the control groups and experiment groups. PirB and GFAP expression were investigated with immunohistochemistry in brain at 30 days after the ih injection of LPS. Double labeling with immunofluorescenee was used to detect whether PirB was expressed not only by neurons but also by glial cells. Results: In the phosphate-buffered saline (PBS)-treated controls, PirB neuron-like cells were mainly observed in the cerebral cortical 4 and 5, with round/ovale or pyramidal shape. PirB staining consisted of brownish reaction products in the membrane of the neurons. At 30 days after unilateral intrahippocampal LPS injection (10 Izg in 4 IA PBS), PirB immunoreactivity was markedly increased in the ipsilateral cerebral cortex of the LPS-injected animals in comparison to those of PBS-injected group. Astrocytes were significantly activated in the piriform cortex and entorhinal cortex of brain, with larger cell body and hypertrophic proces- ses at 30 days after the endotoxin treatment. The increased PirB staining localized in neurons and astrocytes, but did not detect double staining for PirB and CDllb. Conclusion: LPS can elicit up-regulation of PirB expression in neurons and astrocytes in the cortex of rat brain, which may play a potential role in PirB immune-mediated control of the synaptic plasticity changes and the associated functional deficits in learning and memory.
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