It is well established that acute administration of adrenocortical hormones enhances the consolidation of memories of emotional experiences and, concurrently, impairs working memory. These different glucocorticoid effects on these two memory functions have generally been considered to be independently regulated processes. Here we report that a glucocorticoid receptor agonist administered into the medial prefrontal cortex (mPFC) of male Sprague-Dawley rats both enhances memory consolidation and impairs working memory. Both memory effects are mediated by activation of a membrane-bound steroid receptor and depend on noradrenergic activity within the mPFC to increase levels of cAMPdependent protein kinase. These findings provide direct evidence that glucocorticoid effects on both memory consolidation and working memory share a common neural influence within the mPFC.

Noradrenergic activation of the basolateral complex of the amygdala (BLA) modulates the consolidation of memory for many kinds of highly emotionally arousing training tasks. The present experiments investigated whether posttraining noradrenergic activation of the BLA is sufficient to enable memory consolidation of a low-arousing training experience. Sprague-Dawley rats received intra-BLA infusions of norepinephrine, the β-adrenoceptor antagonist propranolol or saline immediately after either 3 or 10 min of object recognition training. Saline-infused controls exhibited poor 24-h retention when given 3 min of object recognition training and good retention when given 10 min of training. Norepinephrine administered after 3 min of object recognition training produced dose-dependent enhancement of 24-h object recognition memory whereas propranolol administered after 10 min of training produced dose-dependent impairment of memory. These findings provide evidence that posttraining noradrenergic activation of the BLA enhances memory of a low-arousing training experience that would otherwise not induce long-term memory. Thus, regardless of the degree of emotional arousal induced by an experience, noradrenergic activation of the BLA after the experience ensures that it will be better remembered. KeywordsNorepinephrine; Propranolol; β-adrenoceptor; Emotional arousal; Memory modulation There is extensive evidence that noradrenergic activation of the basolateral complex of the amygdala (BLA) modulates memory consolidation (McGaugh, 2000;2004;McGaugh & Roozendaal, 2002). Norepinephrine or the β-adrenoceptor agonist clenbuterol infused into the BLA immediately posttraining enhance the memory of many emotionally arousing training tasks, including inhibitory avoidance (Ferry, Roozendaal, & McGaugh, 1999; IntroiniCollison, Miyazaki, & McGaugh, 1991), contextual fear conditioning (Huff, Wright-Hardesty, Higgins, Matus-Amat, & Rudy, 2005;, water-maze spatial training and extinction of contextual fear conditioning (Berlau & McGaugh, 2005). In contrast, posttraining intra-BLA infusions of β-adrenoceptor antagonists impair the consolidation of memory for emotionally arousing training experiences Miranda, LaLumiere, Buen, Bermudez-Rattoni, & McGaugh, Correspondence: James L. McGaugh, 320 QRL -CNLM, UC Irvine, Irvine, CA 92697-3800, Telephone: (949) Fax: (949) 824-2952, EMAIL: JLMCGAUG@UCI.EDU. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. 2003). Such findings strongly suggest that noradrenergic activation of the BLA is critically involved in regulating the consolidation of memory o...

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The segregation of figures from the background is an important step in visual perception. In primary visual cortex, figures evoke stronger activity than backgrounds during a delayed phase of the neuronal responses, but it is unknown how this figure-ground modulation (FGM) arises and whether it is necessary for perception. Here, we show, using optogenetic silencing in mice, that the delayed V1 response phase is necessary for figure-ground segregation. Neurons in higher visual areas also exhibit FGM and optogenetic silencing of higher areas reduced FGM in V1. In V1, figures elicited higher activity of vasoactive intestinal peptide–expressing (VIP) interneurons than the background, whereas figures suppressed somatostatin-positive interneurons, resulting in an increased activation of pyramidal cells. Optogenetic silencing of VIP neurons reduced FGM in V1, indicating that disinhibitory circuits contribute to FGM. Our results provide insight into how lower and higher areas of the visual cortex interact to shape visual perception.