A novel study with mice as the animal model found the effects of alcohol and rapid antidepressants on the brain overlap. Alcohol, the researchers claim, seems to activate the same brain pathway as antidepressant medication. This serves to explain why a drink or two when you’re down can go a long way. However, it also explains why so many of the clinically depressed are alcoholics.
Alcohol self-medication — now we know why
Kimberly Raab-Graham, a researcher at the Wake Forest School of Medicine in Winston-Salem, NC, became intrigued by the potential link between alcohol ingestion and antidepression effects after studying ketamine. Studies have time and time again proved that ketamine, if handled under a specific dosage, is a wonderful antidepressant with effects showing up as early as 2 hours and can last for weeks. See a previous ZME post titled ‘Ketamine might become our secret weapon against depression’ for more.
Ketamine is a drug from a class called N-methyl-D-aspartate (NMDA) antagonists which block NMDA receptors. Alcohol is also a NMDA antagonist so Raab-Graham decided to investigate whether there are any antidepressant qualities in alcohols.
For the study, genetically modified mice who bear depression-like behaviour were used. Raab-Graham and colleagues injected some of them with alcohol — a high-enough dose to induce intoxication — then introduced them to a forced swim test (FST) and slash test. The researchers found that compared to control mice, the tipsy rodents showed a rapid reduction in depression-like behaviour, meaning they tried to swim more.
Interestingly enough, the antidepressant effects were registered up to 24 hours after ingestion suggestion alcohol has long-lasting effect.
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After taking a closer look, the researchers found that a protein called FMRP was involved in alcohol’s blocking of the NMDA receptor. This protein, which is known to be involved in autism, seems to alter the activity of gamma-aminobutyric acid (GABA), turning it into a neurotransmitter. This same pathway is activated in mice who were given rapid antidepressants, leading the team to conclude that the two share the same molecular paradigm.
“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.”