Mechanisms for acute stress-induced enhancement of glutamatergic transmission and working memory.
Mechanisms for acute stress-induced enhancement of glutamatergic transmission and working memory.
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DOI：
10.1038/mp.2010.50
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发表时间：
2011-02
影响因子：
11
通讯作者：
中科院分区：
文献类型：
--
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皮质类固醇应激激素对前额叶皮质（PFC）的功能有很大影响，前额叶皮质是控制认知和情绪的中心区域，尽管其潜在机制尚不清楚。我们发现，行为应激或短期皮质酮治疗在体外诱导的突触反应和NMDARs和AMPAR的表面表达的PFC锥体神经元通过依赖于血清和糖皮质激素诱导激酶（SGK）的诱导和Rab 4，介导早期内体和质膜之间的受体再循环的激活的机制延迟和持续增强。工作记忆，一个关键的功能，依赖于前额叶皮层的神经递质传递，是通过SGK依赖性机制在急性应激动物增强。这些结果表明，急性应激，通过激活糖皮质激素受体（GR），通过SGK/Rab 4信号增加NMDAR和AMPAR的运输和功能，这导致增强的突触传递，从而促进PFC介导的认知过程。
Corticosteroid stress hormones have a strong impact on the function of prefrontal cortex (PFC), a central region controlling cognition and emotion, though the underlying mechanisms are elusive. We found that behavioral stressor or short-term corticosterone treatment in vitro induces a delayed and sustained potentiation of the synaptic response and surface expression of NMDARs and AMPARs in PFC pyramidal neurons via a mechanism depending on the induction of serum- and glucocorticoid-inducible kinase (SGK) and the activation of Rab4, which mediates receptor recycling between early endosomes and the plasma membrane. Working memory, a key function relying on glutamatergic transmission in PFC, is enhanced in acutely stressed animals via a SGK-dependent mechanism. These results suggest that acute stress, by activating glucocorticoid receptors (GRs), increases the trafficking and function of NMDARs and AMPARs via SGK/Rab4 signaling, which leads to the potentiated synaptic transmission, thereby facilitating cognitive processes mediated by the PFC.
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影响因子：
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作者：
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