Mental disorders are the leading causes of disability worldwide. They comprise a broad range of conditions, including mood disorders, which are in general marked by a significant distress, emotional disturbances, social withdrawal and a loss of interest in normally rewarding activities. Stress is a key environmental factor that predisposes to many mood disorders, such as depression and hinders remission. The behavioral sequelae of stress partly result from enduring changes in striatal dopamine and glutamate transmission. Current therapies primarily target symptoms rather than their causes due to our poor knowledge of the mechanisms underlying stress-related mental disorders. We used the chronic social defeated stress paradigm to generate depressive-like symptoms in mice susceptible to stress and also take advantage of the resilient phenotypes to disentangle the molecular adaptations underlying vulnerability to depression. We carried out western blot analyses of punches of nucleus accumbens and caudate putamen on frozen brains to separate and quantify the different subunits of glutamate receptors, as well as examining variation in dopamine receptors as well as PSD95. Using proximity ligation assay, we also examined the physical interaction between dopamine and glutamate receptors (i.e receptor heteromers), as the formation of these complexes is a, important mechanism by which receptors can modify their functions and could be playing a key role in the appearance and maintenance of depressive like symptoms. Overall, our work will provide new evidence for the complex molecular maladaptations occurring in mood disorders.