Glucocorticoids in the prefrontal cortex enhance memory consolidation and impair working memory by a common neural mechanism

Abstract

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.

Infralimbic cortex controls the activity of the hypothalamus–pituitary–adrenal axis and the formation of aversive memory: Effects of environmental enrichment

“…These results suggest that the infralimbic cortex could contribute to the formation of aversive memory, in part, by increasing corticosterone concentrations. The involvement of corticosterone increases, immediately after training, enhancing the formation of aversive memory has been previously reported [36,37].…”

Effects of psychosocial stress on episodic memory updating

“…PFC function is enhanced under low to moderate acute stress (Yuen et al, 2009). Under high stress, norepinephrine levels and dopamine levels rise and shut down the PFC (Arnsten, 2000;Barsegyan, Mackenzie, Kurose, McGaugh, & Roozendaal, 2010;Birnbaum, Podell, & Arnsten, 2000;Roozendaal, McReynolds, McGaugh, 2004). There appears to be a narrow range for optimal norepinephrine (Aston-Jones & Cohen, 2005) and dopamine activity in the PFC (Arnsten & Goldman-Rakic, 1998;Murphy, Arnsten, Goldman-Rakic, & Roth, 1996;Zahrt, Taylor, Mathew, &Arnsten, 1997).…”

“…Memory consolidation via the hippocampus is left relatively intact, to encode stressful events as a survival mechanism (Barsegyan, Mackenzie, Kurose, McGaugh, & Roozendaal, 2010;Liang, 2001;Roozendaal, McReynolds, McGaugh, 2004). As a consequence of this ability to better remember aversive events, our ability to retrieve and modulate information under stress may suffer.…”

Neural mechanisms and computations underlying stress effects on learning and memory

“…Animal studies showed that corticosterone and norepinephrine (NE) act together to facilitate memory formation through actions involving the amygdala, hippocampus, and prefrontal cortex (PFC) [10,12]. More recently, glucocorticoids and the noradrenergic system were shown to interact in the medial PFC in producing working memory impairment [13]. In addition, the capability of these systems to influence learning processes depending on other brain systems -such as the dorsal striatum -was also shown [14].…”