首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Effects of increasing durations of immobilization stress on plasma corticosterone level, learning and memory and hippocampal BDNF gene expression in rats.
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Effects of increasing durations of immobilization stress on plasma corticosterone level, learning and memory and hippocampal BDNF gene expression in rats.

机译:固定应激持续时间的延长对大鼠血浆皮质酮水平,学习记忆和海马BDNF基因表达的影响。

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摘要

Stress effects on learning and memory are widely recognized, but less agreement exists on whether they are positive or negative as well as on their neuronal and neuromolecular correlates. Stress involves expression of certain genes such as neurotrophin BDNF (brain derived neurotrophic factor), which is also involved in learning, but results are not consistent. Here effects of stress on memory and BDNF expression were studied using on adult male rats exposed to "immobilization stress" for various "short" durations, i.e., 1-h, 3-h, 5-h and "long-term" ones (2-h/day for 1 week). Learning and memory was measured using passive avoidance testing (STL=step-through-latency scores) as well as plasma corticosterone (CSt) levels and hippocampal BDNF gene expression. CSt increased in the 3-h and longer stressed groups but differences were significant in the 5-h and 1-week stressed subgroups. Three and 5-h of stress markedly and significantly (60-69%, p<0.01) decreased memory retention in the stressed animals, while 1-h of stress had no effect; prolonged stress (2-h daily for 1-week) increased memory significantly (33%, p<0.05). Hippocampal BDNF gene expression increased in the 1-h and 3-h stressed groups (44%, p<0.05 and 71%, p<0.01); but this parameter steadily declined in the 5-h stressed group (26%, p<0.05) and weeklong stressed group (6%, not significant). Statistical analysis revealed an apparent but significant negative correlation between changes in memory and those of BDNF gene expression, indicating that BDNF may possibly play a compensatory role, reversing deleterious effects of stress on hippocampal memory functions.
机译:压力对学习和记忆的影响已得到广泛认可,但是在它们是正还是负以及它们的神经元和神经分子相关性上,人们的共识较少。压力涉及某些基因的表达,例如神经营养蛋白BDNF(脑源性神经营养因子),这也参与学习,但结果不一致。在这里,我们对成年雄性大鼠在各种“短”持续时间(即1小时,3小时,5小时和“长期”时间)内暴露于“固定压力”的成年雄性大鼠进行了研究,研究了压力对记忆力和BDNF表达的影响(每天2小时/ 1周)。使用被动回避测试(STL =逐步潜伏期得分)以及血浆皮质酮(CSt)水平和海马BDNF基因表达来测量学习和记忆。在3小时和更长的压力组中,CSt增加,但在5小时和1周的压力亚组中,差异显着。应激后3小时和5小时显着且显着(60-69%,p <0.01)降低了应激动物的记忆力,而应激1小时没有影响。长时间的压力(每天2小时,共1周)可显着增加记忆力(33%,p <0.05)。 1 h和3 h应激组海马BDNF基因表达增加(44%,p <0.05和71%,p <0.01);但是在5小时压力组(26%,p <0.05)和为期一周的压力组(6%,不显着)中,该参数稳定下降。统计分析表明,记忆力的变化与BDNF基因表达的变化之间存在明显但显着的负相关性,表明BDNF可能起补偿作用,逆转了应激对海马记忆功能的有害影响。

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