Cocaine addiction: Scientists cure mice of dependency on the drug

Study discovers molecule which drives mice to seek out cocaine - and can be treated with drugs already known to be safe in humans

Treatment significantly lowered desire to search for drug and amount consumed (iStock)

Scientists have found that they can decrease appetite for cocaine by neutralising a protein molecule which is found in the blood and brain at higher levels in repeat cocaine users.

This raises the prospect for a safe medication for cocaine addiction by using existing treatments to tackle this biological system driving drug-taking behaviour.

The protein molecule, G-CSF, affects the reward centres of the brain and could become the first medication to help people beat cocaine addiction according to doctors, from Mont Sinai Medical Centre in New York.

“The results of this study are exciting because outside of 12-step programmes and psychotherapy, no medication-assisted therapy exists to treat cocaine addiction,” according to lead researcher Dr Drew Kiraly, assistant professor of psychiatry at Icahn School of Medicine at Mount Sinai.

The team found that injecting this G-CSF molecule directly into the brain’s reward centres, a region called the “nucleus acumbens”, led to a significant increase in the cocaine seeking and consumption behaviours in mice.

In trials mice treated with G-CSF worked much harder to seek out more cocaine as the strength of each dose was gradually lowered.

This finding is important, according to Dr Kiraly, because there are safe treatments already on the market which target this molecule in humans, primarily for kick-starting production of infection fighting cells after chemotherapy.

When the team tested a treatment which neutralises G-CSF they found they could effectively deaden the mice’s motivation to seek out the drug.

Crucially these changes in G-CSF levels were only linked with cocaine appetite, and the mice saw no change in their interest for other treats, like sugar water, which also stimulate the reward centres of the brain.

This could make it a key to overcoming the dead-ends that have persisted in finding an addiction treatment, despite the signifiant improvements in our understanding of other areas of addiction.

The study, published in Nature Communications, said treatments are hamstrung “for a number of reasons, including problems with side effects, routes of delivery, or abuse potential of agents tested.”

Potential for substance abuse is a risk in several other candidates that are in development, with the risk being that patients are weaned off one addictive substance to another.

“Treatment with a G-CSF modulator would have the distinct advantage that it may be harnessed to reduce drug taking while ostensibly having no abuse potential on its own—a known confound in many previous trials for psychostimulant use disorders,” the authors conclude.

Dr Kiraly admits there is more work to be done to adapt these findings to humans, but that there is a high possibility of it leading to future treatments.

“Drugs that manipulate G-CSF already exist as Food and Drug Administration-approved medications.

“Once we clarify how it can best be targeted to reduce addiction-like behaviours, there is a high possibility that treatments targeting G-CSF could be translated into clinical trials and treatments for patients.”