The increase in 2-AG that occurs in response to repeated restraint stress is transient, and subsides on termination of the stressor. Thus, it is unlikely that the enhanced DSI observed in stressed mice is directly related to stress-induced increases in 2-AG content because slice preparation and recording times were up to several hours after termination of the stressor; that is, it is unlikely that the 2-AG that was elevated during the restraint exposure was still present during recordings. Instead, we suggest that adaptations in one or more enzymatic components of 2-AG metabolism have occurred in response to repeated stress exposure conferring an enhanced capacity of BLA neurons from stressed mice to engage in 2-AG-mediated short-term synaptic plasticity in response to appropriate stimulation, in this case depolarization.
