Glucocorticoids enhance taste aversion memory via actions in the insular cortex and basolateral amygdala

Abstract

It is well established that glucocorticoid hormones strengthen the consolidation of hippocampus-dependent spatial and contextual memory. The present experiments investigated glucocorticoid effects on the long-term formation of conditioned taste aversion (CTA), an associative learning task that does not depend critically on hippocampal function. Corticosterone (1.0 or 3.0 mg/kg) administered subcutaneously to male Sprague-Dawley rats immediately after the pairing of saccharin consumption with the visceral malaise-inducing agent lithium chloride (LiCl) dose-dependently increased aversion to the saccharin taste on a 96-h retention test trial. In a second experiment, rats received corticosterone either immediately after saccharin consumption or after the LiCl injection, when both stimuli were separated by a 3-h time interval, to investigate whether corticosterone enhances memory of the gustatory or visceral stimulus presentation. Consistent with the finding that the LiCl injection, but not saccharin consumption, increases endogenous corticosterone levels, corticosterone selectively enhanced CTA memory when administered after the LiCl injection. Suppression of this training-induced release of corticosterone with the synthesis-inhibitor metyrapone (35 mg/kg) impaired CTA memory, and was dose-dependently reversed by post-training supplementation of corticosterone. Moreover, direct post-training infusions of corticosterone into the insular cortex or basolateral complex of the amygdala, two brain regions that are critically involved in the acquisition and consolidation of CTA, also enhanced CTA retention, whereas post-training infusions into the dorsal hippocampus were ineffective. These findings provide evidence that glucocorticoid effects on memory consolidation are not limited to hippocampus-dependent spatial/contextual information, but that these hormones also modulate memory consolidation of discrete-cue associative learning via actions in other brain regions.

Juvenile Obesity Enhances Emotional Memory and Amygdala Plasticity through Glucocorticoids

“…To determine how HFD exposure during adolescence leads to enhanced consolidation of emotional memories, we investigated the role of glucocorticoids, since previous research has shown that GR activation in the BLA modulates consolidation of emotional memory as well as LTP in lean animals (Roozendaal and McGaugh, 1997;Miranda et al, 2008;Sarabdjitsingh et al, 2012). Moreover, adolescence is a decisive period for maturation of the HPA axis (Spear, 2000;McCormick and Mathews, 2010;Foilb et al, 2011), and previous reports indicate that chronic HFD exposure can alter HPA axis activity (Tannenbaum et al, 1998;Legendre and Harris, 2006;Sharma and Fulton, 2013).…”

mTOR is essential for corticosteroid effects on hippocampal AMPA receptor function and fear memory

“…At the same time rapamycin (6 mg/kg, Sigma) or DMSO (0.01%) was administered i.p. We have used a single dose of corticosterone in a range that mimics plasma corticosterone levels induced by stress and facilitates memory formation (Cordero and Sandi 1998;Miranda et al 2008;Atsak et al 2015). Then, the animals were transferred back into their home cage.…”

Endocannabinoid Signaling within the Basolateral Amygdala Integrates Multiple Stress Hormone Effects on Memory Consolidation

“…This dose of corticosterone results in an increase in circulating corticosterone levels within the physiological range and enhances memory consolidation (Miranda et al, 2008). The corticosterone and SR141716 mixture was dissolved in 5% polyethylene glycol, 5% tween-80, and 5% ethanol in saline.…”