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Naltrexone was first developed in the 1970s as a compound to block heroin and other opioid agonists from activating the receptors for opiates like heroin. In the mid-1980s, naltrexone was approved for the treatment of heroin addiction. In the late 1980s, researchers began to suspect that drinking alcohol was pleasurable because it released endogenous morphine-like molecules. Joseph R. Volpicelli, associate professor and senior scientist at the Treatment Research Center at the University of Pennsylvania, was one of those original researchers.

"The reward system in the brain involves several neurotransmitters," said Volpicelli, "one of which is the opioid neurotransmitter system." Activation of this system - by alcohol consumption, for example - is associated with pain relief, calming and euphoria. "When opioids are stimulated," he said, "that in turn causes an increase in the neurotransmitter called dopamine." Dopamine activity in the brain center called the nucleus accumbens is thought to be key to reward and experiencing the "high" of a variety of different drugs such as cocaine, amphetamines, and nicotine. "What happens is that the brain gets a 'taste' of having endorphins or dopamine released, and it wants more of it," Volpicelli continued. "So first use is like an appetizer for the brain, particularly for people who have a family history of alcoholism and may have a genetic susceptibility for becoming addicted to alcohol. Having a taste of these endogenous opioids is enough to make some people want more of them."

Preclinical research has shown that animals treated with an opioid antagonist such as naltrexone decrease voluntary consumption of alcohol in the laboratory. In human clinical trials, naltrexone
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Contact: Mary E. McCaul, Ph.D.
betsymc@jhmi.edu
410-955-5439
Alcoholism: Clinical & Experimental Research
13-Sep-2000