A new study has provided researchers with deeper insight into the cellular mechanism linked with alcohol dependence.
This signaling pathway has been regulated by a gene, called neurofibromatosis type 1 (Nf1), which The Scripps Research Institute (TSRI) scientists found was linked with excessive drinking in mice. The new research showed that Nf1 regulates gamma-aminobutyric acid (GABA), a neurotransmitter that lowers anxiety and increases feelings of relaxation.
However, the TSRI researchers weren't sure exactly how Nf1 affected the brain. They suspected that Nf1 might be relevant to alcohol-related GABA activity in an area of the brain called the central amygdala, which was important in decision-making and stress- and addiction-related processes.
TSRI Research Associate, Melissa Herman, said that as GABA release in the central amygdala has been shown to be critical in the transition from recreational drinking to alcohol dependence, they thought that Nf1 regulation of GABA release might be relevant to alcohol consumption.
In addition to showing that Nf1 was key to the regulation of the GABA, the research also showed that variations in the human version of the Nf1 gene are linked to alcohol-dependence risk and severity in patients.
The research is published in the journal Biological Psychiatry.