首页> 外文期刊>The European Journal of Neuroscience >Stress alleviates reduced expression of cell adhesion molecules (NCAM, L1), and deficits in learning and corticosterone regulation of apolipoprotein E knockout mice.
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Stress alleviates reduced expression of cell adhesion molecules (NCAM, L1), and deficits in learning and corticosterone regulation of apolipoprotein E knockout mice.

机译:应激减轻了细胞粘附分子(NCAM,L1)的表达减少,并且降低了载脂蛋白E基因敲除小鼠的学习和皮质酮调节能力。

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摘要

Cell adhesion molecules (CAMs) involved in synaptic changes underlying learning and memory processes, are implicated in the effect of stress on behavioural performance. The present study was designed to test the hypothesis that (i) expression of CAMs is apolipoprotein E- (apoE) genotype dependent and (ii) repeated exposure to stress modulates the synthesis of CAMs in an apoE-genotype dependent manner. Using ELISA we tested this hypothesis and measured expression of NCAM and L1 in different brain regions of naive and stressed apolipoprotein E-knockout (apoE0/0) and C57Bl6 (wild-type) mice. Naive apoE0/0 mice had elevated basal morning corticosterone and ACTH concentrations and decreased expression of NCAM and L1 compared to wild-type mice. Repeated exposure of mice to rats, as the common stressor, alleviated the reduction in expression of CAMs in apoE0/0 mice; seven days after the last rat exposure, expression of NCAM was increased in frontal brain and hippocampus whereas expression of L1 was increased in hippocampus and cerebellum. Rat stress attenuated the elevation of basal morning corticosterone concentration in apoE0/0 mice towards concentrations detected in wild-type mice. Moreover, rat stress improved learning and memory of apoE0/0 mice in the water maze. In conclusion, repeated exposure to stress eliminated apoE-genotype-related differences in expression of CAMs. Under these same conditions the differences in cognitive performance and corticosterone concentrations were abolished between wild type and apoE0/0 mice.
机译:涉及学习和记忆过程的突触变化的细胞粘附分子(CAMs)与应激对行为表现的影响有关。本研究旨在测试以下假设:(i)CAMs的表达是载脂蛋白E-(apoE)基因型依赖性的;并且(ii)反复暴露于应激以apoE基因型依赖性的方式调节CAMs的合成。我们使用ELISA检验了这一假设,并测量了天真和应激载脂蛋白E基因敲除(apoE0 / 0)和C57Bl6(野生型)小鼠不同大脑区域中NCAM和L1的表达。与野生型小鼠相比,幼稚的apoE0 / 0小鼠的基础早晨皮质酮和ACTH浓度升高,NCAM和L1的表达降低。小鼠反复暴露于大鼠中,作为常见应激源,减轻了apoE0 / 0小鼠中CAMs表达的降低;在最后一次暴露后的第7天,额叶脑和海马中NCAM的表达增加,而海马和小脑中L1的表达增加。大鼠应激将apoE0 / 0小鼠的基础早上皮质酮浓度的升高减弱到野生型小鼠中检测到的浓度。此外,大鼠应激改善了水迷宫中apoE0 / 0小鼠的学习和记忆。总之,反复暴露于压力消除了CAMs表达中与apoE基因型相关的差异。在这些相同的条件下,野生型和apoE0 / 0小鼠之间认知能力和皮质酮浓度的差异被消除。

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