These findings suggest that administration of Δ9-THC during the early adulthood can potentiate the development of schizophrenia-related behavioral phenotypes induced by neonatal exposure to PCP in mice.
In this sense, electrophysiology and viral vector-based circuit dissection, like optogenetics, can further elucidate how exogenous cannabinoids worsen (e.g., tetrahydrocannabinol, THC) or ameliorate (e.g., cannabidiol, CBD) schizophrenia symptoms, like hallucinations, delusions, and cognitive deficits.
The cognitive abnormalities were prevented in DN-DISC1 mice exposed to Δ<sup>9</sup>-THC by simultaneous adolescent treatment with the cyclooxygenase-2 inhibitor, NS398.