Exposure of the amygdala to elevated levels of corticosterone alters colonic motility in response to acute psychological stress.

The amygdala is important for integrating the emotional, endocrine and autonomic responses to stress. Exposure of the amygdala to elevated levels of corticosterone (CORT) induces anxiety-like behavior and a hypersensitive colon in rodents; however, effects on colonic transit are unknown. Micropellets releasing CORT alone or combined with a selective glucocorticoid (GR) or mineralocorticoid (MR) receptor antagonist were implanted bilaterally at the dorsal boundary of the central amygdala in male rats. Inactive cholesterol implants served as controls. Seven days later, rats received water avoidance stress (WAS) for 1 h and the fecal pellet output was measured. Colorectal transit was also evaluated following the stressor by recording the time for expulsion of a glass bead placed into the colorectum. Plasma CORT levels were evaluated before WAS, after 60 min of WAS and 90 min post-WAS. Exposure of the amygdala to elevated CORT did not alter daily fecal pellet production or the number of fecal pellets released in response to WAS. However, following WAS, rats with CORT implants on the amygdala showed a delay in colorectal transit compared to cholesterol-implanted controls. Plasma CORT measurements showed that basal and WAS-induced increases in plasma CORT were similar in all groups but a prolonged increase in plasma CORT was observed 90 after cessation of WAS in rats with CORT implants. The post-WAS changes in colonic motility and plasma CORT were prevented by antagonism of GR or MR in the amygdala, suggesting their importance in driving stress-associated changes in colonic motility.