MedicalResearch.com Interview with:
Pietro Cottone, Ph.D.
Associate Professor
Departments of Pharmacology and Psychiatry
Laboratory of Addictive Disorders
Boston University School of Medicine Boston, MA 02118
Medical Research: What is the background for this study? What are the main findings?
Dr. Cottone: Binge-eating disorder affects over ten million people in the USA and it is characterized by excessive consumption of junk food within brief periods of time, accompanied by loss of control, uncomfortable fullness and intense feelings of disgust and embarrassment. Increasing evidence suggests that binge-eating disorder can be regarded as an addiction behavior.
Memantine, a neuroprotective drug which blocks the glutamatergic system in the brain, is an
Alzheimer's disease medication, and it has been shown potential to treat a variety of addictive disorders.
We first developed a rodent model of binge eating by providing a sugary, chocolate diet only for one hour a day, while the control group was given the standard laboratory diet. Rats exposed to the sugary diet rapidly develop binge eating behavior, observed as a 4 fold increase in food intake compared to controls. Furthermore, binge eating rats are willing to work to a much greater extent to obtain just the cue associated with the sugary food (not the actual food), as compared to controls. In addition, binge eating subjects exhibit compulsive behavior by putting themselves in a potentially risky situation in order to get to the sugary food, while the control group obviously avoids that risk.
We then tested whether administering memantine could reduce binge eating of the sugary diet, the strength of cues associated with junk food as well as the compulsiveness associated with binge eating. In addition, we studied which area of the brain was mediating the effects of memantine, by injecting the drug directly into the brain of binge eating rats.
Our data show that memantine was able to block
binge eating of the sugary diet, the willingness to work to obtain a cue associated with junk food, as well as the risky behavior of rats when the sugary diet was provided in a potentially unsafe environment. When we injected the drug directly into the nucleus accumbens of rats, they stopped binge eating. Importantly, the drug had no effects in control rats eating a standard laboratory diet.
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