After a hard day at work, a drink or two can often boost a sour mood. Now, a new study may explain why, after finding alcohol has the same effect on the brain as some antidepressants.
Published in the journal Nature Communications, the study shows that alcohol activates the same brain pathway as medications that have been shown to have fast-acting antidepressant effects.
However, the researchers – including principal investigator Kimberly Raab-Graham, Ph.D., of Wake Forest School of Medicine at Wake Forest Baptist Medical Center in Winston-Salem, NC – stress that their findings in no way suggest that individuals with depression should turn to alcohol as a form of treatment.
Instead, the results may help explain why some people with depression take up drinking as a way of coping – a behavior known as the “self-medication hypothesis,” which often leads to alcohol use disorders.
“There’s definitely a danger in self-medicating with alcohol,” says Raab-Graham. “There’s a very fine line between it being helpful and harmful, and at some point during repeated use, self-medication turns into addiction.”
According to the researchers, previous studies have shown that N-methyl-D-aspartate (NMDA) antagonists – drugs that block the activity of NMDA receptors, such as ketamine – may alleviate symptoms of depression in as little as 2 hours, with effects lasting up to 2 weeks.
Because alcohol is also believed to inhibit NMDA receptor activity, the team set out to investigate whether alcohol might also act as an antidepressant.
To reach their findings, the researchers used male mice that had been genetically modified to develop depressive-like behaviors, representative of those that arise in humans.
The mice participated in the forced swim test (FST) and splash test – experiments that identify depressive-like behaviors – and beforehand, some of the rodents were injected with a single high dose of alcohol, enough to induce intoxication.
The team found that, compared with the control group, the mice that were treated with alcohol showed a rapid reduction in depressive-like behaviors, similar to that seen in mice given a rapid antidepressant.
What is more, the reduction in depressive-like behaviors was present at 24 hours after alcohol administration, suggesting it has a long-lasting effect.
On further investigation, the researchers found that after blocking NMDA receptor activity, alcohol worked with a protein called FMRP – known to be involved in autism – in order to alter the activity of gamma-aminobutyric acid (GABA), turning it into a neurotransmitter.
The same brain pathways were activated in mice administered with rapid antidepressants, the team notes.
Commenting on what the results show, the authors write:
“[…] our data define a common molecular paradigm for alcohol and rapid antidepressants, and identify a mechanism for the initial antidepressant effects of alcohol.
A shift in [GABA receptor] signaling is observed with both rapid antidepressants and acute ethanol treatment, which may provide insight into the molecular basis for the high comorbidity between major depressive disorder and AUD [alcohol use disorder].”
While further research is needed to explore the link between alcohol use and depression, the team says these current findings help shed light on the issue.
“Because of the high comorbidity between major depressive disorder and alcoholism there is the widely recognized self-medication hypothesis, suggesting that depressed individuals may turn to drinking as a means to treat their depression,” says Raab-Graham. “We now have biochemical and behavioral data to support that hypothesis.”