Adolescent exposure to THC, the main psychoactive component of cannabis, increases the risk of later neuropsychiatric symptoms, and the medial prefrontal cortex is a key brain region involved. The antioxidant N-acetylcysteine (NAC) prevented cognitive, synaptic, neuronal, and neurochemical deficits caused by chronic adolescent THC exposure in a rodent model. This suggests that THC-induced oxidative stress contributes to neuropsychiatric risk and identifies NAC as a potential preventive treatment.
Adolescent female rats exposed to THC gained weight slower than controls during treatment. In adulthood, they showed no behavioral abnormalities in tests of locomotion, sensorimotor gating, memory, or anxiety. However, long-lasting molecular adaptations occurred: altered expression of estrogen receptor-α and fatty acid amid hydrolase in the hypothalamus and hippocampus, along with enduring changes in hippocampal oscillatory patterns. These sex-specific adaptations may protect females against the long-term behavioral abnormalities consistently seen in male cohorts.