Alcohol followed the same biochemical pathway as rapid antidepressants ultimately transforming an acid from an inhibitor to a stimulator of neural activity.
Alcoholism is linked with a perceived need to self-medicate as, few alcoholic beverages influence the same neural reactions asrapidly effective antidepressants. The study, published in the latest issue of Nature Communications, tested doses of intoxicating levels of alcohol on an animal model. Researchers observed the alcohol followed the same biochemical pathway as rapid antidepressants such as Ketamine, ultimately transforming an acid called GABA from an inhibitor to a stimulator of neural activity.
‘Depressed individuals may turn to drinking as a means to treat their depression as doses of intoxicating levels of alcohol acts as a stimulant of neural activity.’
Test subjects were shown to exhibit non-depressive behavior lasting at least 24 hours.Principal investigator Kimberly Raab-Graham, an associate professor of physiology and pharmacology at Wake Forest School of Medicine, says her team's experiments strongly support the self-medication hypothesis.
"Because of the high co-morbidity 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," she said. "We now have biochemical and behavioral data to support that hypothesis."
Raab-Graham cautioned, however, that relying on the intoxicating substance can still pose a threat.
"There's definitely a danger in self-medicating with alcohol," she added. "There's a very fine line between it being helpful and harmful, and at some point during repeated use self-medication turns into addiction."
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