The cannabinoid 1 receptor (CB1R) is abundant in the hippocampus and linked to schizophrenia risk when cannabis is used during adolescence. In rats, adolescent pre-treatment with the CB1R agonist CP-55940 caused a lasting decrease in hippocampal theta oscillations in adulthood, a brain rhythm essential for memory and cognition. The impairment was more severe when exposure occurred in early adolescence (postnatal days 32–36) compared to late adolescence (days 42–46). These findings suggest that early adolescence is a critical window during which cannabis exposure can permanently disrupt neural network synchronization, potentially increasing vulnerability to psychiatric disorders.
Adolescent exposure to a cannabis-like compound (CP-55940) in rats causes lasting abnormalities in brain theta oscillations during adulthood. Theta oscillations are crucial for memory and cognition, and their disruption is linked to psychiatric disorders. Rats given the compound during early adolescence (postnatal days 32-36) showed a significantly greater reduction in theta power in adulthood compared to those treated later (postnatal days 42-46). This suggests that early adolescence is a particularly vulnerable period for cannabis-induced changes in brain function, potentially increasing sensitivity to cannabinoids later in life.