News Release

Cocaine use may alter brain cells, play role in depression

Peer-Reviewed Publication

NIH/National Institute on Drug Abuse

A study by researchers from the University of Michigan and the Ann Arbor Veterans Affairs Medical Center suggests that chronic cocaine use may cause damage to brain cells that help produce feelings of pleasure, which may contribute, in part, to the high rates of depression reported among cocaine abusers. It is well-known that cocaine increases levels of the brain chemical dopamine, resulting in the "high" that abusers feel. Prolonged use of the drug, however, may reduce dopamine levels, making it harder for abusers to experience positive feelings.

Dr. Karley Little, lead investigator, and colleagues studied samples of brain tissue obtained during autopsies of 35 long-term cocaine users and 35 non-users. They analyzed the tissue for dopamine and the protein VMAT2, which is found in dopamine transporters. Urine or serum samples were also analyzed for the presence of cocaine, opioids, antidepressants, and antipsychotic medications. A person close to each individual was interviewed about the individual's substance abuse, alcoholism, and symptoms of personality and mood disorders.

Researchers found that cocaine users had lower concentrations of dopamine and VMAT2 in their brains than did non-users. Additionally, cocaine users suffering from depression had lower levels of VMAT2 than those who were not depressed. Dr. Little and colleagues were uncertain whether dopamine cells had been destroyed or just dysregulated by cocaine use, and if such changes could be reversed.

  • WHAT IT MEANS: These findings suggest that chronic cocaine use may cause changes in the brain that could make it harder for a person to feel a sense of pleasure. Further efforts at clarifying the detrimental effects of cocaine on brain cells may help in the development of effective treatment interventions and pharmacotherapies.
  • This study, funded in part by the National Institute on Drug Abuse, was published in the January 2003 issue of the American Journal of Psychiatry.

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