Mechanisms for acute stress-induced enhancement of glutamatergic transmission and working memory

被引：0
作者：
E Y Yuen
W Liu
I N Karatsoreos
Y Ren
J Feng
B S McEwen
Z Yan
机构：
[1] School of Medicine and Biomedical Sciences,Department of Physiology and Biophysics
[2] State University of New York at Buffalo,undefined
[3] Laboratory of Neuroendocrinology,undefined
[4] The Rockefeller University,undefined
来源：
Molecular Psychiatry | 2011年 / 16卷
关键词：
acute stress; corticosterone; NMDA receptors; AMPA receptors; SGK; Rab4; working memory;
D O I：
暂无
中图分类号：
学科分类号：
摘要：
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 N-methyl-D-aspartic acid receptors (NMDARs) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) in PFC pyramidal neurons through 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 through an SGK-dependent mechanism. These results suggest that acute stress, by activating glucocorticoid receptors, increases the trafficking and function of NMDARs and AMPARs through SGK/Rab4 signaling, which leads to the potentiated synaptic transmission, thereby facilitating cognitive processes mediated by the PFC.
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页码：156 / 170
页数：14
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