Stress may lead to increased alcohol consumption due changes in the brain's reward system, a new study has found, paving way for new therapies to treat alcohol addiction as well as post-traumatic stress disorder.
The brain chemistry underlying interactions between stress and alcohol remain largely unknown. Reinforcement of addictive substance use and stress signalling involves common neural systems, including the brain reward centre.
A team led by John Dani from the University of Pennsylvania in the US, found that rodents that had been exposed to stress had a weakened alcohol-induced dopamine response and voluntarily drank more alcohol compared to controls.
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.
Stress alters the intricate system of checks and balances in the firing and quiescence of many types of neurons.
"These effects happen at the minute level of potassium, chloride, and other ions moving across the neuron outer membrane via channels and transporters," Dani said.
"In addition, by chemically blocking stress hormone receptors on neurons, we prevented stress from causing increased drinking behaviour," he said.
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 controls, and the increase was maintained for several weeks.
"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 said.
After the stress, the reward circuitry looked normal at first glance when they examined the rats' neurons, researchers said.
However, if the circuits were strongly used, in this case via consumption of ethanol, alterations to neurons were noticeable and the dopamine response to alcohol was blunted.
The change in neuron physiology means that a specific set of neurons that are normally inhibitory flip and become excitatory. This flip alters the rats' response to ethanol, making them consume more and more.
To reverse the negative effects of the erroneous excitatory signal, the team chemically prevented the excitatory switch within the reward circuitry.
This correction prevented the blunted alcohol-induced dopamine signal, causing the stressed rats to consume less alcohol.
"We gave the rats a chemical called CLP290 to restore the stress-altered circuitry to normal, which in turn corrected the firing of the dopamine neurons," said Dani.
"This line of research has implications for people with PTSD who have an increased risk for over-use of alcohol and drugs," he said.
The findings were published in the journal Neuron.
Disclaimer: No Business Standard Journalist was involved in creation of this content
