(New York -Jan. 16, 2018) -- Mount Sinai researchers have identified a protein produced by the immune system--granulocyte-colony stimulating factor (G-CSF)--that could be responsible for the development of cocaine addiction.
A study showed that G-CSF can alter a mouse's desire for cocaine, but not for other rewards. This effect is modulated by a brain region that plays a central role in reward processing and addiction. If applicable to humans, these findings represent a potential therapeutic approach to decrease a cocaine addict's motivation to seek the drug without introducing a potential new substance for abuse.
The results of the study will be published online in Nature Communications.
Previous research has demonstrated a link between cocaine use and the immune system in humans and animals, with addicts showing altered immune responses to drugs and drug cues. In this study, the research team identified G-CSF--a cytokine produced by immune cells which was expressed at higher levels in both the blood and brain in mice that were treated with repeated doses of cocaine --. Injecting G-CSF into the nucleus accumbens, a brain region associated with reward, causes mice to take more cocaine, but does not change their motivation to consume a more natural reward, sugar water. Conversely, injecting an antibody that neutralizes G-CSF in the nucleus accumbens can reduce the mouse's motivation to take cocaine. Taken together, the results from this study suggest that manipulating G-CSF in the reward center of the brain changes the biochemical signals that push animals to take cocaine.
"The results of this study are exciting because outside of 12-step programs and psychotherapy, no medication-assisted therapy exists to treat cocaine addiction," said the study's senior author, Drew Kiraly, MD, PhD, Assistant Professor of Psychiatry at Icahn School of Medicine at Mount Sinai. "Drugs that manipulate G-CSF already exist as FDA-approved medications. Once we clarify how G-CSF signaling can best be targeted to reduce addiction-like behaviors, there is a high possibility that treatments targeting G-CSF could be translated into clinical trials and treatments for patients."
This study was supported by NIH grants DA044308, P01-DA008227 and DA042111 and from funds for the Brain and Behavior Research Foundation, the Leon Levy Foundation, and the Seaver Family Foundation.
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