ME is a high-affinity ligand for both MOR and DOR67 and is therefore likely to inhibit the BLA-Im synapse. Exogenous ME (10–30 μM) significantly inhibited the eEPSC amplitude (Fig. 2f,g) and increased the PPR (Fig. 2h). Both DOR and MOR selective antagonists produced a partial reversal of ME inhibition and together they fully reversed both the ME induced inhibition (Fig. 2i) and change in PPR (baseline: 1.3±0.1; ME: 1.8±0.2; ICI+CTAP: 1.2±0.2; n=8, P>0.05 baseline versus ICI+CTAP, paired t-test). Unsurprisingly, given the low affinity of ME for KOR67 we found norBNI had no effect on the ME inhibition (Fig. 2i). Thus, exogenous ME inhibited glutamate release at the BLA-Im synapse through activation of both MOR and DOR, which is consistent with the receptor pharmacology of ME67 and the opioid sensitivity of the BLA-Im synapse, as defined above.