Scientists Characterize, Target, & Manipulate Critical Subset of Neurons Responsible for Excessive Drinking; Major Breakthrough in Identifying Key Brain Cells May Open Door to Developing Drug Therapies or Even Gene Therapies for Alcohol Addiction

Scientists at Scripps Research Institute (La Jolla, California) have found that they can reverse the desire to drink in alcohol-dependent rats--with the flip of a switch. The researchers were able to use lasers to temporarily inactivate a specific neuronal population, reversing alcohol-seeking behavior and even reducing the physical symptoms of withdrawal. "This discovery is exciting--it means we have another piece of the puzzle to explain the neural mechanism driving alcohol consumption," says Olivier George, PhD, an Associate Professor at Scripps Research and senior author of the new study, published on March 18, 2019 in Nature Communications. The open-access article is titled “Inactivation of a CRF-Dependent Amygdalofugal Pathway Reverses Addiction-Like Behaviors in Alcohol-Dependent Rats.” Although the laser treatment is far from ready for human use, Dr. George believes identifying these neurons opens the door to developing drug therapies or even gene therapies for alcohol addiction. "We need compounds that are specific to this neuronal circuitry," Dr. George says. According to the National Institute on Alcohol Abuse and Alcoholism, more than 15.1 million adults in the United States suffer from alcohol use disorder. Previous work at Scripps Research has shown that transitioning from casual drinking to dependent drinking occurs alongside fundamental changes in how the brain sends signals. These signals drive the intense cravings that make it so difficult for many people to scale back their alcohol consumption. Dr. George and his colleagues have been hunting for the brain cells that driving drinking in an alcohol-addicted rat model. In 2016, they reported that they had found a possible source: a neuronal "ensemble," or group of connected cells in a brain region called the central nucleus of the amygdala (CeA).
Login Or Register To Read Full Story