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Roots of Alcohol Dependence?

Researchers link a gene already tied to alcohol dependence with a neurotransmitter involved in anxiety and relaxation.

By | August 27, 2014

WIKIMEDIA, XLIBBERThe neurofibromatosis type 1 (Nf1) gene, which has been previously linked to alcohol dependence, may exert its influence on alcohol intake through the regulation of gamma-aminobutyric acid (GABA), a neurotransmitter known to decrease anxiety and boost feelings of relaxation, according to a mouse study published this month (August 18) in Biological Psychiatry. The research, led by scientists at The Scripps Research Institute (TSRI), also links variations in the human Nf1 with the risk and severity of alcohol dependence.

“Despite a significant genetic contribution to alcohol dependence, few risk genes have been identified to date, and their mechanisms of action are generally poorly understood,” coauthor Vez Repunte-Canonigo said in a press release.

The team decided to look for a connection with the neurotransmitter GABA as a result of previous work that has shown GABA release in the central amygdala, a brain area involved in decision making, stress, and addiction, is “critical in the transition from recreational drinking to alcohol dependence,” said coauthor Melissa Herman. Examining mouse models of alcohol dependence, the team found that mice with functional Nf1 genes started to increase their alcohol intake after a single period of withdrawal, while those with one copy of the gene knocked out did not increase their ethanol consumption. Moreover, in heterozygous Nf1 mice, intake of alcohol did not result in higher GABA release in the central amygdala, which was observed in mice with two functional copies of the Nf1 gene.

The researchers also explored variation in human Nf1 using data from some 9,000 people and found the gene correlated alcohol-dependence risk and severity. “A better understanding of the molecular processes involved in the transition to alcohol dependence will foster novel strategies for prevention and therapy,” coauthor Pietro Paolo Sanna said in the release.

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