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.
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.