Our biochemical data suggest that repeated restraint exposure results in adaptations in 2-AG metabolism that confers BLA neurons with an enhanced capacity to elevate 2-AG levels. We therefore tested the hypothesis that this increased capacity translates into an enhanced ability of BLA neurons to participate in eCB-mediated synaptic signaling. We examined DSI, an eCB-mediated form of short-term plasticity we showed to be mediated by 2-AG, in control mice and those exposed to either 1 or 10 days of restraint stress. Our data indicate that acute 1 h restraint exposure does not effect DSI magnitude or duration compared with control mice, consistent with our biochemical data that acute restraint stress does not alter 2-AG or precursor DAG levels in the BLA. However, exposure to 10 days of restraint stress, which increased 2-AG and DAG levels, increased DSI duration, without effecting maximal DSI magnitude. Longer duration recordings at 0.33 Hz exhibited a run-down, thus we were not able to accurately determine the duration of DSI in stressed mice under these conditions. The duration of eIPSC depression in stressed mice remains an important
