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Why Reformed Cocaine Addicts Can Relapse

Brain behaves differently in craving and reward

THURSDAY, May 10 (HealthScout) -- The brain chemistry that makes a reformed cocaine addict relapse is different from what causes addiction in the first place, researchers report.

"This opens a whole broad range of therapeutic possibilities," says Dr. Stanislav R. Vorel, a neuroscientist at Albert Einstein College of Medicine in New York City and leader of researchers reporting the finding in the May 11 issue of Science.

The study, involving addicted rats, makes clear the distinction between the "reward" brain mechanism that leads to addiction and the "craving" mechanism that causes a continuing yearning for the drug and can make a reformed addict go bad, he says.

One critical difference is that the main chemical involved in craving is not dopamine, a molecule that transmits signals between brain cells in the reward circuit; instead it is glutamine, a different neurotransmitter working in a different pathway.

Rats in the study were first given access to cocaine intravenously and were able to get their fixes by hitting levers in their cages. When the apparatus was altered to deliver salt water rather than cocaine, the rats stopped pressing the levers after a week.

The "reward" or addictive part of the brain is the medial forebrain bundle, where nerve cells use dopamine for communication, Vorel says. But when the researchers stimulated a different part of the brain, the glutamine-using ventral subiculum of the hippocampus that is associated with memory, the rats went back to pushing the levers with fervor.

"The idea is that the area of the brain we designated for study has a whole different chemical makeup than the area usually studied in regards to relapse," says Vorel, who received his medical degree in the Netherlands and now is a graduate student at Einstein.

What is true for laboratory animals almost certainly is true for humans, Vorel says, except that relapse for human addicts is caused by some outside influence, such as an emotional situation or a visual cue (for example, spending a night with old friends who used the drug). Relapse thus could be prevented in tempting situations with medication that blocks glutamine activity, Vorel says. One glutamine blocker, kynurenic acid, had that effect in the test animals, he says.

No glutamine blockers are available now for human treatment, says Peter Kalivas, professor and chairman of physiology and neurology studies at the Medical College of South Carolina in Charleston. "But an area of active interest for pharmaceutical companies is to find a way to modify glutamate activity to treat craving," he says.

"This is potentially a new slant on how we might handle addiction," Kalivas says.

Dopamine is also part of the craving response, he says. "Probably what is going on is that the memory areas of the brain become involved in relapse and trigger the areas of the brain involved with reward. The big distinction is that there is more cortical involvement in relapse than in reward," Kalivas says.

The brain imaging technique used in the animal study can help shed new light on human addiction, Vorel says. "When a stimulus is presented, we can do an MRI [magnetic resonance imaging] or CAT [computerized tomography] scan to study brain activity," he says.

He says such studies could help answer "one big question: Whether these results would also be true for heroin or other addictions."

What To Do

The government reports cocaine abuse has been on the decline in recent years, but it remains a problem. If you're trying to kick this habit or stay clean, you'll have to stick to the tried-and-true methods until some benefit comes from this research.

For detailed information on addiction and its treatment, look at the National Institute on Drug Abuse. And if you need assistance, try Cocaine Anonymous or Drug Help.

Or, read previous HealthScout articles on cocaine and drug addiction.

SOURCES: Interviews with Stanislav R. Vorel, neuroscientist, Albert Einstein College of Medicine, New York City, and Peter Kalivas, chairman and professor of physiology and neurology, Medical College of South Carolina, Charleston; May 11, 2001 Science
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