There is growing evidence that tonic ECB signaling in the BLA and elsewhere is mediated by AEA, whereas phasic ECB responses to robust neuronal activation are sub-served by 2-AG [53–56]. Interestingly, stress appears to produce divergent effects on AEA and 2-AG levels in the BLA – with an elevation in 2-AG levels [57], but a rapid induction of FAAH activity and a resultant decline in the pool of AEA [58–60] were reported following exposure to various types of stress. These differing directional and temporal responses probably indicate a difference in the mechanisms modulating the effects of these two ECBs and their catabolic enzymes in the BLA. These mechanisms are not currently understood, however, and it is also unclear exactly how the relative balance between changes in AEA and 2-AG impacts the response and recovery from stress.
