LIPOPOLYSACCHARIDE INDUCES PAIRED IMMUNOGLOBULIN-LIKE RECEPTOR B (PIRB) EXPRESSION, SYNAPTIC ALTERATION, AND LEARNING-MEMORY DEFICIT IN RATS
LIPOPOLYSACCHARIDE INDUCES PAIRED IMMUNOGLOBULIN-LIKE RECEPTOR B (PIRB) EXPRESSION, SYNAPTIC ALTERATION, AND LEARNING-MEMORY DEFICIT IN RATS
复制标题
DOI：
10.1016/j.neuroscience.2012.02.022
复制
发表时间：
2012-05-03
期刊：
影响因子：
3.3
通讯作者：
Li, Z.
中科院分区：
文献类型：
--
作者：
Deng, X. -. H.;Ai, W. -M.;Li, Z.
一些典型的免疫蛋白在神经系统中表达，其中成对免疫球蛋白样受体B（Pir B）是主要组织相容性复合物I类抗原（MHC-I）的受体，但可能通过抑制突触可塑性而在脑中对神经元回路的稳定性起生理作用。慢性神经炎症在许多神经退行性疾病中是常见的，并且通常与神经元/突触损伤和功能障碍相关。在这里，我们研究了PirB在大鼠脑内应用脂多糖（LPS），这已被证明会诱导促炎性变化和认知障碍的啮齿动物的大脑中的表达。单侧海马内注射LPS（10 μ g溶于4 μ l磷酸盐缓冲盐水，PBS）1个月后，相对于载体（PBS）对照，在实验组的同侧海马结构和皮质中检测到PirB的蛋白水平和免疫反应性增加。PirB标记的增加定位于星形胶质细胞和神经元。与对照组相比，脂多糖处理大鼠同侧海马结构和皮质中的突触素蛋白水平和免疫反应性也有所降低。Morris水迷宫实验表明LPS处理的动物的海马依赖性空间学习和记忆受损。我们的研究结果增加了新的实验数据，在内毒素诱导的神经炎症，突触改变和认知能力下降的模型中，大脑神经元和神经胶质细胞中的免疫蛋白上调。结果表明，PirB调制可能参与神经退行性疾病条件下的病理过程。(C)2012年IBRO。由爱思唯尔有限公司出版。保留所有权利。
Some typical immune proteins are expressed in the nervous system, among which the paired-immunoglobulin-like receptor B (PirB) is a receptor for major histocompatibility complex class I antigen (MHC-I), but may play a physiological role in the brain for neuronal circuitry stability by inhibiting synaptic plasticity. Chronic neuroinflammation is common to many neurodegenerative diseases and is often associated with neuronal/synaptic damage and dysfunction. Here we examined the expression of PirB in the rat brain following intracerebral application of lipopolysaccharide (LPS), which has been shown to induce proinflammatory changes and cognitive deficits in rodents. One month after unilateral intrahippocampal LPS injection (10 mu g in 4 mu l phosphate-buffered saline, PBS), increased protein levels and immunoreactivity of PirB were detected in the ipsilateral hippocampal formation and cortex of the experimental group relative to vehicle (PBS) control. The increased PirB labeling was localized to astrocytes and neurons. Reduced synaptophysin protein levels and immunoreactivity were also found in the ipsilateral hippocampal formation and cortex in LPS-treated rats relative to controls. Morris water maze tests indicated that hippocampus-dependent spatial learning and memory were impaired in LPS-treated animals. Our findings add new experimental data for an upregulation of immune proteins in neuronal and glial cells in the brain in a model of endotoxin-induced neuroinflammation, synaptic alteration, and cognitive decline. The results suggest that PirB modulation may be involved in the pathological process under neurodegenerative conditions. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.