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Scientists Have Found A Way To Protect Mice Against Cocaine Addiction


Stephen Luntz

Stephen has a science degree with a major in physics, an arts degree with majors in English Literature and History and Philosophy of Science and a Graduate Diploma in Science Communication.

Freelance Writer

A molecule has been found that reduces cocaine consumption among mice. It could one day be used to help people addicted to cocaine. Wayne Abraham/Shutterstock

Mice who have had a certain gene removed consume less cocaine, when given the chance, than unmodified rodents. A drug that blocks the molecule produced by this gene reduces cocaine consumption in genetically normal mice. The finding is exciting because not only do humans have a matching gene, but past studies have implicated it in risks for many drug addictions, cocaine included, raising the prospects of a broadscale treatment for drug addiction.

Despite the ferocity of denial from contributors to our Facebook comments section whenever IFLScience reports on the research, there is abundant evidence that genetics play a role in addiction. Many other factors are also important, but people with certain genetic variations are at much greater risk of becoming hooked on drugs than everyone else.


Past genetic comparisons of people with cocaine addictions and the wider population have revealed the importance of genes associated with the receptor-type protein tyrosine phosphatase D (PTPRD) molecule. People with genetic variations that reduce PTPRD production are less likely to become addicted than those with the more common form. Dr George Uhl of the University of New Mexico confirmed the PTPRB gene's significance by knocking out one copy of the gene in some mice, and comparing them with counterparts with two versions.

In the Proceedings of the National Academy of Sciences, Uhl reports the single-copy mice responded to the availability of cocaine by consuming about 70 percent as much of it as their counterparts. Encouraged by this discovery, Uhl and his co-authors identified the molecule 7-butoxy illudalic acid analog (7-BIA) as one that inhibits PTPRB’s activity, while apparently having little effect on other biomolecules.

Uhl gave 7-BIA to mice prior to allowing them to press a lever to administer themselves a hit of coke. Non-treated mice gave themselves the maximum bump, or nearly so, 80 percent of the time. Those previously given 7-BIA only took as much snow as they could get 48 percent of the time.

The mice in question had already been exposed to cocaine to the point of maximizing their dosage, suggesting 7-BIA can assist those who are already addicted, not just provide pre-exposure protection against addiction.


Most 7-BIA-treated mice still liked a fix, but were often happy with smaller doses.

Uhl did not observe any side effects of the treatment, but notes 7-BIA's low solubility may justify a search for a similar, but more easily administered, molecule.

A treatment for cocaine addiction would be valuable enough, but Uhl's work may have much wider applications. PTPRB has been associated with low success in quitting smoking, as well as alcohol and amphetamine consumption. If 7-BIA is safe, it may make it easier for people to beat all forms of drug addiction, saving lives on an epic scale.


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