The RGS6 protein (regulator of G protein signaling 6) uses two separate mechanisms to control the behavior leading need for alcohol and death of cells in heart, liver, and other organs.
The study was published in the journal PNAS.
“Given the prevalence of alcohol abuse worldwide there is a clear need for more effective therapeutics,” said lead researcher Rory Fisher from the University of Iowa. “We propose that inhibiting this RGS6 protein could represent a new approach to counteract alcohol dependence and at the same time protect against the cell-killing actions of alcohol in the heart and liver.”
In his previous work performed at his lab, Fisher suggested that RGS5 might be involved in signaling pathways in the brain that are involved in addiction and alcohol dependence.
The study, having Adele Stewart as first author and Biswanath Maity, used mice without RGS6 to assess the role of the protein in both alcohol need and organ damage. Scientists found that mice lacking RGS6 protein used less alcohol than wild-type mice when allowed access to alcohol.
Additionally, mice lacking the protein RGS6 were less likely to crave the alcohol-induced reward, and had less severe and much shorter alcohol withdrawal symptoms.
“To our knowledge RGS6 is the only gene with a demonstrated ability to promote alcohol-seeking behaviours while simultaneously worsening the damaging effects of alcohol consumption on the heart, stomach, intestine and liver,” Fisher said.
In the brain, RSG6 is involved in alcohol craving by controlling levels of dopamine, a neurotransmitter associated with addiction and reward-seeking behavior.
In the heart and liver, RSG6’s effect is based on its role in a pathway that causes cell death through production of damaging compounds called reactive oxygen species.