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.
Los investigadores patrocinados por el NIDA mostraron que, en los monos, la metanfetamina altera las estructuras cerebrales involucradas en la toma de decisiones y afecta negativamente la capacidad de eliminar los comportamientos habituales que se han vuelto inútiles o contraproducentes.
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.
Two researchers share their reasons for researching transcranial magnetic stimulation (TMS) for treating cocaine addiction, and describe challenges to moving forward this potentially promising therapy.
In mice, a cocaine-induced imbalance in the activity of two key populations of neurons in the reward system persists for a longer period after repeated exposure to the drug. For long-term users, this change could both weaken the cocaine “high” and strengthen the compulsion to seek the drug.