In the striatum, intense stimulation (five antidromic depolarizations, 100 Hz) results in opioid inhibition of glutamate release that is maximal 500 ms after the stimulus13. Guided by this, we delivered a short train of stimuli (‘moderate' stimulus, 5 stimuli, 150 Hz) followed by a single ‘test' stimulus (500 ms interval) to the BLA (Fig. 3a). Unless otherwise noted, we analysed opioid effects on the test eEPSC. Using this protocol, we found that naloxone significantly increased the amplitude of the test eEPSC (Fig. 3c,i), indicating the moderate stimulus induces endogenous opioid release. We wondered whether opioid release occurs with lower stimulation but due to peptide degradation, we were unable to detect the opioid effect. To test this, we assessed whether inhibition of opioid peptide degradation could reveal an opioid effect during low stimulation. Enkephalin, the most likely opioid to be acting at this synapse, is catabolized by at least three zinc metalloproteases38. We tested whether a cocktail of peptidase inhibitors targeting these enzymes (thiorphan, 10 μM; captopril, 1 μM and bestatin, 10 μM; Fig. 3d), could increase endogenous opioid inhibition. This peptidase inhibitor cocktail significantly enhanced the effects of exogenously applied, submaximal ME (300–500 nM) on eEPSC amplitude (Fig. 3e,f), confirming these peptidases act to break down exogenous ME and thus limit its actions at the BLA-Im synapse.