While these data are quite compelling, they are limited by the fact that these studies are performed in an amphibian species which may behave physiologically different than a mammalian system. However, a recent study demonstrated the cross-species relevance of this phenomenon by revealing that endocannabinoid signalling in the amygdala is involved in the effects of glucocorticoids on aversive memory consolidation (Campolongo et al., 2009). It has been previously reported that systemic administration of glucocorticoids can facilitate the consolidation of aversive memories through a rapid action in the amygdala that involves a reduction in GABAergic neurotransmission (Roozendaal et al., 2009). This study illustrated mediation of this phenomenon by endocannabinoid signalling, in that local administration of a CB1 receptor antagonist into the basolateral amygdala immediately prior to administration of corticosterone mitigated that ability of corticosterone to facilitate aversive memory consolidation (Campolongo et al., 2009). Taken together with our recent biochemical findings, these data indicate that glucocorticoids (in the absence of stress) are capable of promoting endocannabinoid mobilization (likely AEA) within the amygdala to modulate local synaptic transmitter release and influence behavioural responses to environmental stimuli.
