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In Acb neurons, the NMDA NR1 (NR1) subunit is coexpressed not only with the dopamine D1 receptor (D1R), but also with the \u00b5\u2010opioid receptor (\u00b5\u2010OR), which mediates certain behaviors that are adversely impacted by schizophrenia. The NMDA\u2010NR1 subunit has been suggested to play a role in the D1R trafficking and behavioral dysfunctions resulting from systemic administration of apomorphine, a D1R and dopamine D2 receptor agonist that impacts prepulse inhibition to auditory\u2010evoked startle (AS). Together, this evidence suggests that the NMDA receptor may regulate D1R trafficking in Acb neurons, including those expressing \u00b5\u2010OR, in animals exposed to auditory startle and apomorphine. We tested this hypothesis by combining spatial\u2010temporal gene deletion technology, dual labeling immunocytochemistry, and behavioral analysis. Deleting NR1 in Acb neurons prevented the increase in the dendritic density of plasma membrane D1Rs in single D1R and dual (D1R and \u00b5\u2010OR) labeled dendrites in the Acb in response to apomorphine and AS. Deleting NR1 also attenuated the decrease in AS induced by apomorphine. In the absence of apomorphine and startle, deletion of Acb NR1 diminished social interaction, without affecting novel object recognition, or open field activity. These results suggest that NR1 expression in the Acb is essential for apomorphine\u2010induced D1R surface trafficking, as well as auditory startle and social behaviors that are impaired in multiple psychiatric disorders. 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