Specificity in learning is crucial for our survival, ensuring knowledge is applied when needed, especially in the context of fear learning. Dysfunctions in these learning mechanisms can lead to undesirable responses and behaviours such as addiction or anxiety. Studies in both humans and rodents highlight opioids as a key neuromodulator inhibiting fear learning, while dopamine signalling in the amygdala is thought to induce synaptic plasticity, strengthening synapses and driving fear learning. The amygdalo-striatal transition zone (AST) is an enkephalin rich region receiving input from the medial geniculate nucleus (MGM) during fear learning and also activated by foot shock. The AST containing neurons with D1 or D2 receptors positions it as a potential site of opioid dopamine interaction. However, how endogenous opioids are released and interact with dopamine during fear conditioning remains unknown. Using electrophysiology and optogenetics in brain slices from male Sprague-Dawley rats, we asked whether MGM activity induces endogenous opioid release in the amygdala and whether the AST is the source. We observed that the opioid antagonist naloxone increased the synaptic responses following a train of stimuli (28.5±11.1%, n=6) whereas a single stimulus did not (4.55±3.98%, n=8), suggesting opioid release is driven by MGM activity. Furthermore, data from the fluorescent opioid sensor δ-light suggests the AST as the source, with opioid release modulated by dopamine. Knocking down proenkephalin in vivo further indicates that opioids in the AST are critical for fear learning. These findings highlight the importance of endogenous opioid release in the AST in the fear learning process.