"Using a series of genetic and pharmacological approaches, we identified how a compound in the brain, Neuropeptide Y (NPY), can suppress this dangerous behaviour," explained Thomas L Kash, assistant professor at University of North Carolina's (UNC) school of medicine.

The team found that NPY acted in a part of the brain known as the extended amygdala that is linked to both stress and reward.This anti-drinking effect was due to increasing inhibition (the brakes) on a specific population of cells that produce a 'pro-drinking' molecule called corticotropin releasing factor (CRF).

"When we mimicked the actions of NPY using engineered proteins, we were also able to suppress binge alcohol drinking in mice," Kash noted.

Finally, the team found that this anti-drinking NPY system is altered by long-term alcohol drinking in multiple species, suggesting that this may be either a marker or treatment for alcohol abuse.

The identification of where in the brain and how NPY blunts binge drinking and the observation that the NPY system is compromised during early binge drinking prior to the transition to dependence, are novel and important observations.

The study was published online in the journal Nature Neuroscience.


Latest News from Lifestyle News Desk