Prone to binge drinking? This might be why
26 October, 2018
Why do some people only have one drink, whereas others find it difficult to stop? A neuroscientific study sheds light.
According to the most recent estimates, over 15 million adults in the United States — or over 6 percent of the population — have alcohol use disorder.
Approximately 88,000 people die from alcohol-related problems every year, making alcohol the "third leading preventable cause of death" in the United States.
In addition to alcohol dependence, alcohol brings about a number of other disorders, including liver cirrhosis and various forms of cancer.
However, what makes some of us crave alcohol so much, even when it's bad for us? One answer is dopamine, the so-called sex, drugs, and rock 'n' roll neurotransmitter.
Dopamine helps the brain learn new things, but it may also lead us down the path of addiction.
Dopamine earned its nickname because it is a feel-good chemical that is released as a reward for the brain when we learn new things or during pleasurable activities such as sex. It is also the substance that "tells" us to prolong the pleasure and continue to "chase the high."
In the case of alcohol dependence, when alcohol reaches the brain, it causes the neurons in a region called the ventral tegmental area (VTA) to release dopamine.
Until now, the precise molecular steps through which this occurred weren't clear. So, researchers at the Center for Alcohol Research in Epigenetics at the University of Illinois at Chicago (UIC) set out to investigate, and their findings shed new light on binge drinking and alcohol use disorder.
Mark Brodie, a professor of physiology and biophysics in the UIC College of Medicine, is the lead author of the study, which was published in the journal Neuropharmacology.
The effects of KCNK13 channel deficiency
Prof. Brodie and his team started from the hypothesis that alcohol may inhibit a potassium channel called KCNK13. This channel can be found inside the membrane of dopamine neurons in the VTA. So, when this pathway is blocked, neurons release more dopamine than usual.
To verify their hypothesis, the researchers performed a range of experiments. In one of them, the scientists created a mouse model in which KCNK13 was genetically reduced by 15 percent.
The KCNK13-deprived mice drank 20–30 percent more alcohol than their normal counterparts.
Prof. Brodie explains the findings, saying, "We believe that mice with less KCNK13 in the VTA drank more alcohol in order to achieve the same 'reward' from alcohol as normal mice, presumably because alcohol was triggering the release of less dopamine in their brains."
Another experiment focused on the neuronal response to alcohol in the VTA region for mice with less KCNK13.
These neurons were 50 percent less excited in response to ethanol when compared with normal VTA neurons that were exposed to ethanol.
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