The amygdala is central to our emotional responses1. In particular, anxiety and fear learning rely on neural circuits and synaptic plasticity within the amygdala12. These anxiety and fear responses are modulated by our endogenous opioid system. Deleting one family of endogenous opioids, the enkephalins, increases behavioural measures of fear and anxiety34, whereas inhibiting enkephalin breakdown reduces these behaviours5. This suggests that endogenous enkephalin is anxiolytic. However, enkephalin is an agonist at both the μ-opioid receptor (MOR) and δ-opioid receptor (DOR)67 and the consequence of activating each receptor results in opposing behavioural outcomes. Indeed activation of DOR is anxiolytic589, while activation of MOR is anxiogenic910. Given this complexity, understanding the cellular actions of endogenous opioids at the DOR and MOR in the amygdala is critical if we hope to utilize opioid related therapy for emotional disorders. However, while endogenous opioids regulate fear and many other behaviours, including: pain, decision making, drug dependence and memory11, their cellular actions in the brain are poorly understood. Previous studies in various brain regions suggest endogenous opioid regulation of synaptic activity requires intense stimulation1213 and often this is shown to regulate long-term plasticity of synapses121415161718, rather than normal synaptic transmission. This has been taken to suggest that endogenously released opioids regulate learning rather than continuous information flow through a dynamic neural circuit19. However, it is an open question whether endogenously released opioids produce this myriad of behavioural responses solely through the regulation of synapses under intense neuronal activity (such as during learning), or whether regulation under basal conditions also contributes.