Single prolonged stress enhances hippocampal glucocorticoid receptor and phosphorylated protein kinase B levels.
Single prolonged stress enhances hippocampal glucocorticoid receptor and phosphorylated protein kinase B levels.
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DOI：
10.1016/j.neures.2012.11.001
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发表时间：
2013-02
影响因子：
2.9
通讯作者：
Perrine SA
中科院分区：
文献类型：
--
作者：
Eagle AL;Knox D;Roberts MM;Mulo K;Liberzon I;Galloway MP;Perrine SA
创伤后应激障碍（PTSD）的动物模型可以探索创伤增强恐惧和焦虑反应的神经生物学机制。单次长时间应激（SPS）在产生PTSD样行为方面显示出良好的有效性。虽然SPS诱导的行为已被链接到增强糖皮质激素受体（GR）的表达，增强GR表达的分子分支尚未被确定。磷酸化蛋白激酶B（pAkt）在应激介导的广泛性焦虑和记忆增强中是关键的，并且可能受GR调节。然而，目前尚不清楚pAkt水平是否受SPS调节，以及GR和pAkt相关变化的特异性是否有助于SPS后的焦虑样行为。目前的研究着手研究SPS对杏仁核和海马中GR和pAkt蛋白水平的影响，并研究这些变化对非条件性焦虑样行为的特异性。GR和pAkt水平在海马中增加，但杏仁核中没有。此外，SPS对非条件性焦虑样行为没有影响，表明SPS后并没有持续观察到广泛性焦虑。结果表明，SPS增强的GR表达与Akt的磷酸化有关，也表明这些变化与致焦虑表型无关。
Animal models of posttraumatic stress disorder (PTSD) can explore neurobiological mechanisms by which trauma enhances fear and anxiety reactivity. Single prolonged stress (SPS) shows good validity in producing PTSD-like behavior. While SPS-induced behaviors have been linked to enhanced glucocorticoid receptor (GR) expression, the molecular ramifications of enhanced GR expression have yet to be identified. Phosphorylated protein kinase B (pAkt) is critical for stress-mediated enhancement in general anxiety and memory, and may be regulated by GRs. However, it is currently unknown if pAkt levels are modulated by SPS, as well as if the specificity of GR and pAkt related changes contribute to anxiety-like behavior after SPS. The current study set out to examine the effects of SPS on GR and pAkt protein levels in the amygdala and hippocampus and to examine the specificity of these changes to unconditioned anxiety-like behavior. Levels of GR and pAkt were increased in the hippocampus, but not amygdala. Furthermore, SPS had no effect on unconditioned anxiety-like behavior suggesting that generalized anxiety is not consistently observed following SPS. The results suggest that SPS-enhanced GR expression is associated with phosphorylation of Akt, and also suggest that these changes are not related to an anxiogenic phenotype.
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