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.
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.
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.
High-frequency electrical stimulation of neurons deep in the brain can reduce rats’ relapse-like behavior and motivation to take heroin. The finding strengthens hope that deep brain stimulation might offer a new treatment alternative for opioid addiction, particularly for patients who have not benefited from other treatments.