We first introduce the functional role of FAAH within the wider ECB system. Next, we discuss evidence from pharmacological and genetic approaches that loss/inhibition of FAAH function can both mitigate behavioral and neural sequelae of stress and promote learned reductions in fear via actions in the basolateral amygdala (BLA), a central node within the neural circuitry mediating stress and anxiety. We conclude with an outlook for the field going forward and pose some outstanding questions that remain to be addressed.
