To further determine if these effects of acute stress are mediated by glucocorticoid secretion, we subsequently examined the effects of glucocorticoid administration (in the absence of a stressor) on endocannabinoid content within these same limbic structures. Much to our surprise, a single administration of corticosterone was found to robustly increase AEA content within the amygdala, hippocampus and hypothalamus at only 10 min following administration (Hill et al., 2009b). 2-AG content was also found to be elevated 10 minutes following corticosterone administration, but only within the hypothalamus (Hill et al., 2009b) At 1 hour following administration of corticosterone, these effects had almost entirely subsided (Hill et al., 2009b). These data corresponded quite well with the in vitro findings of Tasker and colleagues and demonstrated that in vivo, glucocorticoids (likely acting through a non-genomic mechanism) evoked a rapid induction of endocannabinoid signaling within limbic structures in rats.
