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 a general impairment in 2-AG signaling because receptor-driven eCB release initiated by 50 µM dihydroxyphenylglycine (~50% eIPSC suppression) is comparable to that observed in BLA and other brain regions (Patel and Winder, unpublished data; (Azad et al, 2004)). Thus, it seems that the small magnitude of DSI is attributable to a specific impairment in calcium-dependent eCB synthesis and/or efflux. It is unlikely that high 2-AG degradation rates contribute to the reduced DSI magnitude because pharmacological blockade of MGL activity did not significantly increase maximal DSI.
