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Adolescent Cannabinoid Exposure Induces a Persistent Sub‐Cortical Hyper‐Dopaminergic State and Associated Molecular Adaptations in the Prefrontal Cortex

Abstract Considerable evidence suggests that adolescent exposure to delta‐9‐tetrahydrocanabinol (THC), the psychoactive component in marijuana, increases the risk of developing schizophrenia‐related symptoms in early adulthood. In the present study, we used a combination of behavioral and molecular analyses with in vivo neuronal electrophysiology to compare the long‐term effects of adolescent versus adulthood THC exposure in rats. We report that adolescent, but not adult, THC exposure induces long‐term neuropsychiatric‐like phenotypes similar to those observed in clinical populations. Thus, adolescent THC exposure induced behavioral abnormalities resembling positive and negative schizophrenia‐related endophenotypes and a state of neuronal hyperactivity in the mesocorticolimbic dopamine (DA) pathway. Furthermore, we observed profound alterations in several prefrontal cortical molecular pathways consistent with sub‐cortical DAergic dysregulation. Our findings demonstrate a profound dissociation in relative risk profiles for adolescent versus adulthood exposure to THC in terms of neuronal, behavioral, and molecular markers resembling neuropsychiatric pathology.