Exposing adolescent rats to THC disrupted normal maturation of a key set of neurons in a brain area that corresponds to the human prefrontal cortex. The disruptions produced structural differences that resemble patterns which have been observed in people with addiction and schizophrenia.
These findings add to research showing that nicotine and cannabis have interactive effects on brain structure and function. They also suggest that specialized treatment interventions may be appropriate for people who use both drugs.
People with cannabis dependence have changes in neural circuitry in brain regions related to reward processing, habit formation, and psychopathology. These changes in neural circuitry may provide a useful marker for tracking psychopathology associated with cannabis misuse.
This study demonstrated that cocaine increases expression of the protein E2F3a in the brain’s reward system. The changes in E2F3a levels in the nucleus accumbens are tied to addiction-related behaviors and to altered gene expression.
This research traced the effects of cocaine-induced disruption of serotonin regulation in the ventral pallidum and orbitofrontal cortex. The findings suggest that these effects may contribute to drug-seeking and cocaine-associated cognitive impairments.
Cocaine produces a portion of its rewarding effects by increasing levels of granulocyte-colony stimulating factor (G-CSF) in the brain’s reward center. Treatments that prevent G-CSF signaling in the nucleus accumbens might reduce motivation to use cocaine.
Some teens' marijuana use has been linked to disrupted communication between two key regions in the brain’s reward circuitry at age 20. Disrupted communication between the regions was associated with poorer psychosocial functioning at age 22.