Yuen Eunice Y, Liu Wenhua, Karatsoreos Ilia N, Feng Jian, McEwen Bruce S, Yan Zhen
Department of Physiology and Biophysics, State University of New York at Buffalo, School of Medicine and Biomedical Sciences, Buffalo, NY 14214, USA.
Proc Natl Acad Sci U S A. 2009 Aug 18;106(33):14075-9. doi: 10.1073/pnas.0906791106. Epub 2009 Jul 29.
The prefrontal cortex (PFC), a key brain region controlling cognition and emotion, is strongly influenced by stress. While chronic stress often produces detrimental effects on these measures, acute stress has been shown to enhance learning and memory, predominantly through the action of corticosteroid stress hormones. We used a combination of electrophysiological, biochemical, and behavioral approaches in an effort to identify the cellular targets of acute stress. We found that behavioral stressors in vivo cause a long-lasting potentiation of NMDAR- and AMPAR-mediated synaptic currents via glucocorticoid receptors (GRs) selectively in PFC pyramidal neurons. This effect is accompanied by increased surface expression of NMDAR and AMPAR subunits in acutely stressed animals. Furthermore, behavioral tests indicate that working memory, a key function relying on recurrent excitation within networks of PFC neurons, is enhanced by acute stress via a GR-dependent mechanism. These results have identified a form of long-term potentiation of synaptic transmission induced by natural stimuli in vivo, providing a potential molecular and cellular mechanism for the beneficial effects of acute stress on cognitive processes subserved by PFC.
前额叶皮质（PFC）是控制认知和情绪的关键脑区，受到压力的强烈影响。虽然慢性压力通常会对这些指标产生有害影响，但急性压力已被证明能增强学习和记忆，主要是通过皮质类固醇应激激素的作用。我们采用电生理、生化和行为学方法相结合的方式，试图确定急性压力的细胞靶点。我们发现，体内的行为应激源通过糖皮质激素受体（GRs）在PFC锥体神经元中选择性地引起NMDAR和AMPAR介导的突触电流的长期增强。这种效应伴随着急性应激动物中NMDAR和AMPAR亚基表面表达的增加。此外，行为测试表明，工作记忆是依赖于PFC神经元网络内反复兴奋的关键功能，急性压力通过GR依赖机制增强了工作记忆。这些结果确定了一种体内自然刺激诱导的突触传递长期增强形式，为急性压力对PFC所支持的认知过程产生有益影响提供了潜在的分子和细胞机制。
