One of the main glutamatergic inputs to Im neurons is from pyramidal neurons of the BLA. BLA-Im synapses (Im referred to as medial ventral ITC in ref. 16) in mice have recently been shown to be insensitive to regulation by MOR16, however, it is not known whether this holds across different species. We therefore tested the sensitivity of this synapse to all three opioid receptors. To do this we made whole-cell patch recordings from Im neurons and routinely performed post hoc biocytin staining of the patched cells. As expected, staining revealed small bipolar neurons, with an abundance of dendritic spines, located in a cell dense region ventromedial to the BLA (Fig. 2a)2636. We electrically stimulated the BLA (Fig. 2b) and recorded the resulting evoked excitatory postsynaptic current (eEPSC) in Im neurons. We found BLA-Im eEPSCs were inhibited by selective agonists for DOR (Deltorphin II, 300 nM) or MOR (DAMGO, 1 μM; Fig. 2c,d), which was accompanied with an increase in the paired pulse ratio (PPR, Fig. 2e). Both effects were fully reversed by the selective DOR (ICI174864, 1 μM) and MOR (CTAP, 1 μM) antagonists respectively (Fig. 2c–e). In contrast, neither the κ-opioid receptor (KOR) agonist (U69593, 3 μM) nor antagonist (norBNI, 10 nM) affected the eEPSC amplitude or PPR (Fig. 2c–e). These data indicate the BLA-Im synapse is strongly inhibited through DOR and MOR and the associated increases in PPR indicates the likely site of action is through pre-synaptic reductions in glutamate release. This opioid sensitivity is consistent with the high expression of DOR mRNA in BLA neurons21 and the expression of MOR in BLA pyramidal neurons34 but does differ from the recently reported MOR insensitivity of this synapse described in mice16, suggesting there may be inter-species variability in opioid action within the Im.