Together, these findings, with the observation that the D1R-GluN1 physical interaction reciprocally regulates D1R and NMDAR surface expression and function, prompts the question of whether it is the initial failure in glutamatergic signaling that leads to reduced dopaminergic neurotransmission in schizophrenia through perturbed protein (receptor)-NMDAR interactions in the NMDAR complex. This evidence concerns the gene DRD1 and schizophrenia.