DSI is a widespread form of eCB-mediated short-term synaptic plasticity expressed by neocortical, allocortical, striatal, midbrain, and cerebellar neurons (Kano et al, 2009). DSI has been recently described in BLA slices and dissociated neurons from postnatal rats (Zhu and Lovinger, 2005). As in other brain regions, DSI in the BLA is blocked by CB1 receptor antagonists and intracellular calcium chelation, indicating mediation by calcium-dependent eCB signaling (Zhu and Lovinger, 2005). We extend these findings to show that DSI is present in the mature mouse BLA; however, the magnitude of suppression (~20%) is far less than seen in hippocampus (Wilson and Nicoll, 2001) or cerebellum (Kreitzer and Regehr, 2001), but consistent with data from postnatal rat BLA slices (Zhu and Lovinger, 2005). The relatively small magnitude of DSI in this region is not because of a lack of functional CB1 receptors, because exogenous application of the CB1 agonist Win 55212-2 produced a robust ~50% suppression of eIPSC amplitude in the BLA, which is consistent with earlier data (Azad et al, 2003; Katona et al, 2001). It is also not because of
