Scientists could “turn off” alcohol cravings

It’s nearing midnight and you’ve spent a productive day in Brody. You’ve had dinner, but you’re feeling a bit hungry after all the time working on that assignment for that class you have. All of a sudden, you get a craving — French fries. Cravings are a common occurrence, but have you ever wondered exactly what it is that drives them?

A new research study conducted by the Scripps Research Institute in Florida pinpoints the brain circuit that may be responsible for inciting cravings, specifically alcohol cravings. The study was published on March 18 in Nature Communications. 

Olivier George, who is an associate professor at Scripps Research and a senior author on the paper, believes these findings have important consequences. 

“This discovery is exciting — it means we have another piece of the puzzle to explain the neural mechanism driving alcohol consumption,” George said in a press release.

Researchers discovered that it was possible to reverse the craving for a drink in alcohol-dependent rats — quite literally with the flip of a switch via lasers. A green laser was used to temporarily inactivate a neuronal population that in effect reversed alcohol-seeking behavior and reduced the physical symptoms of withdrawal. This population is located in the central nucleus of the amygdala (CeA).

Such results have a number of positive implications that present possible solutions to alcoholism. Though this laser treatment is nowhere near ready to be administered to the human population, there is much hope for future applications, particularly in the development of drug or gene therapies to combat alcohol addiction. 

George said the treatment needed to be engineered specifically for humans before use. 

“We need compounds that are specific to this neuronal circuitry,” he said. 

The National Institute on Alcohol Abuse and Alcoholism reports that there are currently more than 15.1 million adults in the United States that suffer from an alcohol condition. According to the published article, alcohol addiction is defined as “a chronic relapsing disorder [with close associations to] compulsive drinking, the loss of control over intake, and the emergence of a negative emotional state during abstinence from alcohol.”

Sarah Allen Benton, author of the book Understanding the High-Functioning Alcoholic, estimates that up to half of all alcoholics are the high-functioning type, where the abuse may manifest for decades until an alcohol-related crisis takes place to serve as a wake-up call.

Previous studies have demonstrated a physical link in the transition from casual drinking to dependent drinking in the form of altered brain signals. The new work shows that corticotropin-releasing factor (CRF) neurons comprise 80 percent of the neuronal ensemble related to alcohol cravings.

The research study was conducted by inducing alcohol dependence in rats over the course of several months by a gradual increase in consumption. The rats were surgically implanted with optic fibers aimed to shine light on the CRF neurons. The presence or absence of light would control cells in living tissue.

The alcohol-dependent rats experienced withdrawal symptoms once there was no available alcohol and drank more than ever when the CeA neuronal ensemble was active, but when the green lasers inactivated the CRF neurons, the rats resumed their pre-dependent drinking levels. Symptoms associated with withdrawal, including shaking and abnormal gait, were also visibly reduced. Turning off the laser and reactivating the CRF neurons reinstated the dependent drinking levels.

Giordano de Guglielmo, the first author of the study and a staff scientist at Scripps Research, commented on the research process. 

“In this multidisciplinary study, we were able to characterize, target and manipulate a critical subset of neurons responsible for excessive drinking,” he said. “This was a team effort, and while we used challenging techniques, working with experts in the field and with the right tools, made everything easier and enjoyable.”