Preferential consumption of alcohol in mice results from mutations in specific ion channels that mediate neurotransmission, reports a study in Nature Communications this week. These findings provide new insights into the different mechanisms involved in some forms of alcohol addiction.
GABA ion channels are essential for the normal functioning of the mammalian nervous system. Previous studies suggest that alcohol may exert an effect on some types of GABA ion channels that enhances their activity and contributes to an increase in alcohol-seeking behaviour. However, this hypothesis has not been conclusively proven. To address this, Quentin Anstee and colleagues study two transgenic mouse lines that have mutations in a specific type of GABA receptor. They find that these mice display increased alcohol consumption and self-administration, and are also characterised by GABA channels that can open spontaneously. This change in opening activity alters the excitability of neurons in the mouse brain nucleus accumbens, an area that is heavily implicated in reward and addiction.
Although these studies were carried out in mice, the authors hope that these findings may translate to humans, where mutations in GABA ion channels have been implicated in alcohol dependence in humans. If similar findings are made in humans they may lead to the development of drugs that target some forms of alcohol dependence.