Dec. 27, 2001 CHAPEL HILL -- One of the brain’s natural painkillers -- beta endorphin -- increases significantly in response to alcohol, cocaine and amphetamine drug administration in a key region of the brain that controls addiction, researchers have discovered.
The work, conducted in rats, strongly suggests that the same thing occurs in humans, the scientists say. It offers what could be important new clues in the fight against alcohol and drug addiction.
A report on the findings appears as a rapid communication in the newest issue of the Journal of Neuroscience.
Authors of the paper include Drs. M. Foster Olive of the University of California at San Francisco and Clyde W. Hodge of the University of North Carolina at Chapel Hill.
"This is the first demonstration that drugs of abuse increase beta endorphin levels in a key part of the brain that influences addiction," said senior author Hodge, associate professor of psychiatry at the UNC School of Medicine. "The name of this important forebrain region is the nucleus accumbens. We and others had suspected this response, but it had never been proven until now because methods were not available to test it.
"In this latest work, Dr. Olive adapted a technique for quantifying endorphins and used it to measure how one of the brain’s natural painkillers responds to addicting drugs."
For at least four decades, biomedical researchers have known based on animal studies that certain regions of the brain, when stimulated, produced pleasurable effects, said Hodge, also a member of UNC’s Bowles Center for Alcohol Studies. Those "rewards" promote substance use initially, and eventually, habitual users find it hard to function without them.
About 15 or so years ago, scientists discovered that in those brain regions drugs of abuse caused an elevation in the neurotransmitter compound dopamine, he said. Such knowledge helps them pin down how abused substances affect humans and narrows the search for compounds that can block cravings without harming addicted people.
The researchers administered alcohol, cocaine, amphetamine, nicotine and an inactive salt solution to laboratory rats via injections twice at three-hour intervals. Then, using a technique known as microdialysis combined with solid-phase radioimmunoassay, they measured endorphin levels in brain fluids removed from awake and active rats and found the effect in rodents given the first three drugs.
"We hypothesize that this drug-induced release of endorphins may contribute to the positive reinforcing and motivating properties of alcohol and psychostimulant drugs," Hodge said. "We did not find this same boost in endorphins in this brain region with nicotine, but we don’t know why. It could be that the dose of nicotine we used was too low or that nicotine does not cause this same effect and instead acts in some other way."
Additional research will show whether nicotine increases beta endorphin in the nucleus accumbens or whether it acts on different systems, he said. Such information should contribute to efforts to help people stop smoking.
"This new work also offers a useful technique for evaluating some of the more pertinent questions such as is beta endorphin elevated during craving or during drug self-administration?" Hodge said. "That would suggest that this is a system that could be targeted for development of medications that might help humans deal with the problem of drug addiction."
Future experiments will determine whether the same effect exists in brain if rats actively consume drugs on their own when given the chance, which they usually do.
The research was supported by funds from the state of California for medical research on alcohol and substance abuse through the University of California at San Francisco.
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