Rise in alcohol consumption increases during stress: Study

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New York: Increased stress can cause changes in brain's reward centre, which may then lead to a rise in alcohol consumption, a study, with implications to post-traumatic stress disorder (PTSD), has found.

In the study, researchers used a rat model to explore the relationship between stress signalling and addictive substance use.

Rodents that had been exposed to stress had a weakened alcohol-induced dopamine response and voluntarily drank more alcohol compared to the control group. 

"These effects happen at the minute level of potassium, chloride, and other ions moving across the neuron outer membrane via channels and transporters," John Dani, from the University of Pennsylvania, US. 

"In addition, by chemically blocking stress hormone receptors on neurons, we prevented stress from causing increased drinking behaviour," Dani added. 

The findings may help develop treatment methods for individuals with post-traumatic stress disorder (PTSD), a mental disease characterised by impulsive behaviour and often heavy substance abuse. 

"The research has implications for people with PTSD who have an increased risk for over-use of alcohol and drugs," Dani said.

For the study, rats were exposed to an acute stress for one hour, and then 15 hours later, researchers measured the amount of sugar water laced with ethanol that the mice drank. 

The stressed rats drank significantly more than the control group, and the increase was maintained for several weeks.

The blunted dopamine signalling to ethanol arose due to changes in the circuitry in the ventral tegmental area, the heart of the brain's reward system, the researchers observed. 

"The stress response evolved to protect us, but addictive drugs use those mechanisms and trick our brains to keep us coming back for more," Dani added.

Neurons in the experimental group were found to become more excitable over time, driving the rats to consume more ethanol-laced water. 

After the scientists introduced a chemical called CLP290, stress-altered circuitry returned to normal, the researchers noted in the paper published in the journal Neuron.