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Regulation of Mood by Dopamine D1 Receptors on Cerebral Cortical Interneurons

Depression is a multifactorial brain disorder caused by a variety of alterations in neural structure and function. We have used the Cre/loxP system to selectively delete dopamine D1 receptors from GABAergic neurons from the Nkx2.1 lineage within the medial ganglionic eminence (GABA‐D1‐cKO), which include a subset of crucial cerebral cortical interneurons within the frontal cortex. Cell‐type specific loss of D1 receptor expression was validated by in situ hybridization. Neurobehavioral analyses of GABA‐D1‐cKO mice revealed normal patterns of locomotor activity, anxiety, and spatial and nonspatial memory. However, GABA‐D1‐cKO mice exhibit decreased immobility in the forced swim test and decreased latency to consume a palatable liquid in a novel stressful environment; these are both indicative of an antidepressant‐like effect. GABA‐D1‐cKO mice also show reduced basal plasma corticosterone levels and down‐regulation of the neurexin Cntnap4 in cerebral cortical interneurons. Conditional deletion of dopamine D1 receptors from telencephalic glutamatergic neurons (using Emx1‐Cre as a deletor) does not induce these phenotypes. These data suggest a new mechanism by which cerebral cortical interneurons may contribute to mood regulation and identify a new potential mechanism to exploit in the treatment and prevention of this prevalent brain disorder.