This presented dissertation addresses the molecular and cellular mechanisms of cocaine addiction. Our team previously showed the development of addiction-like behaviour in mice depends on co-activation of glutamate NMDA receptors (NMDAR) and dopamine-1 receptors (D1R), and the ERK signalling pathway. My hypothesis was that the physical interaction between the D1R and NMDAR would be critical in cocaine-induced adaptations. This hypothesis was supported, as co-stimulation of the D1R and NMDAR favoured their physical interactions in cultured neurons. After I developed a peptide (TAT-GluN1C1) that specifically obstructs the association of the receptors, I found treating neurons with TAT-GluN1C1 inhibited the activation of the ERK pathway specifically downstream of co-stimulation of the D1R and NMDAR, but not when either receptor was individually stimulated. Furthermore, this physical interaction has functional consequences, as dissociation of the receptors prevented the D1R from potentiating NMDAR mediated synaptic transmission in brain slices. In vivo, the peptide prevented locomotor sensitisation, the progressive and long-lasting augmentation of cocaine's stimulant effects observable as increased motor activity, in mice. Altogether, these results demonstrate for the first time a novel role for D1R/NMDAR physical interactions in cocaine-induced signalling, plasticity and long term behavioural adaptations that may also be necessary for the persistence of other drug-associated behaviours.