Addiction is a highly debilitating condition consisting of compulsive self-administration and seek for the substance of abuse, and its most challenging feature is the high rate of relapse. Addiction and relapse share similarities with a brain process called neural plasticity which acts through the Brain-Derived Neurotrophic Factor and its receptor TrkB. Moreover, Somatostatin (SST) expressing interneurons are involved in neuronal plasticity and are important in modulating cocaine-seeking behaviour in mice.We are testing the role of TrkB in Somatostatin(SST)-expressing neurons in the formation and extinction of cocaine-seeking behaviour, using mice in which TrkB has been knocked out specifically in SST neurons. We have observed that in these mice, cocaine conditioning is slightly reduced and its extinction through behavioural training is impaired, showing how the acquisition of a cocaine-seeking behaviour and its extinction rely on neural plasticity in SST neurons.We then activated plasticity using a light-activable TrkB in SST neurons in the prefrontal cortex (area involved in the cocaine-seeking suppression) of cocaine-conditioned mice, during extinction training, to promote local neural plasticity and prevent relapse of cocaine-seeking in the mouse model. Identifying the network behind the extinction of reward-seeking behaviour and the role of synaptic plasticity will shed light on targets for new treatments to prevent relapse and improve the outcomes of addiction treatments.