The main findings of study are that (1) the 2-AG synthetic enzyme DAGL∝ is heterogeneously expressed in the amygdaloid complex with the highest levels observed in the BLA, CeAL, and ICMs. (2) 2-AG and precursor DAG levels are increased by repeated, but not acute restraint stress exposure, whereas AA levels are reduced by both acute and repeated restraint stress. (3) Exposure to repeated, but not acute, restraint stress enhances DSI duration in BLA neurons. (4) Repeated restraint stress and the 2-AG degradation inhibitor MAFP produce mutually occlusive prolongation of DSI, suggesting a mechanism involving impaired 2-AG catabolism could subserve these effects. These data suggest that repeated stress exposure confers BLA neurons with an enhanced capacity to elevate 2-AG in response to subsequent stress exposure, and that this enhanced capacity to elevate 2-AG levels is associated with enhanced 2-AG-mediated short-term synaptic suppression of GABAergic transmission in the BLA.
