Alcohol,rapid antidepressants same effects on the brain
Can having a few drinks help people with clinical depression feel better?
Yes. At least in terms of biochemistry.
In a study published in the current issue of the journal Nature Communications, researchers found that alcohol produces the same neural and molecular changes as drugs that have proven to be rapidly effective antidepressants.
"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," said the study's principal investigator, Kimberly Raab-Graham, Ph.D., associate professor of physiology and pharmacology at Wake Forest School of Medicine, part of Wake Forest Baptist Medical Center. "We now have biochemical and behavioral data to support that hypothesis." This, however, does not at all suggest that alcohol can be regarded as an effective treatment for depression.
"There's definitely a danger in self-medicating with alcohol," Raab-Graham said. "There's a very fine line between it being helpful and harmful, and at some point during repeated use self-medication turns into addiction." In their study using an animal model, Raab-Graham and her colleagues found that a single dose of an intoxicating level of alcohol, which has been shown to block NMDA receptors (proteins associated with learning and memory), worked in conjunction with the autism-related protein FMRP to transform an acid called GABA from an inhibitor to a stimulator of neural activity. In addition, the research team found that these biochemical changes resulted in non-depressive behavior lasting at least 24 hours.
This study demonstrated that alcohol followed the same biochemical pathway as rapid antidepressants in the animals, while producing behavioral effects comparable to those observed in people. In recent years, single doses of rapid antidepressants such as Ketamine have proven capable of relieving depressive symptoms within hours and lasting for up to two weeks, even in individuals who are resistant to traditional antidepressants.
"Additional research is needed in this area, but our findings do provide a biological basis for the natural human instinct to self-medicate," Raab-Graham said. "They also define a molecular mechanism that may be a critical contributor to the comorbidity that occurs with alcohol use disorder and major depressive disorder."
In a study published in the current issue of the journal Nature Communications, researchers found that alcohol produces the same neural and molecular changes as drugs that have proven to be rapidly effective antidepressants.
"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," said the study's principal investigator, Kimberly Raab-Graham, Ph.D., associate professor of physiology and pharmacology at Wake Forest School of Medicine, part of Wake Forest Baptist Medical Center. "We now have biochemical and behavioral data to support that hypothesis." This, however, does not at all suggest that alcohol can be regarded as an effective treatment for depression.
"There's definitely a danger in self-medicating with alcohol," Raab-Graham said. "There's a very fine line between it being helpful and harmful, and at some point during repeated use self-medication turns into addiction." In their study using an animal model, Raab-Graham and her colleagues found that a single dose of an intoxicating level of alcohol, which has been shown to block NMDA receptors (proteins associated with learning and memory), worked in conjunction with the autism-related protein FMRP to transform an acid called GABA from an inhibitor to a stimulator of neural activity. In addition, the research team found that these biochemical changes resulted in non-depressive behavior lasting at least 24 hours.
This study demonstrated that alcohol followed the same biochemical pathway as rapid antidepressants in the animals, while producing behavioral effects comparable to those observed in people. In recent years, single doses of rapid antidepressants such as Ketamine have proven capable of relieving depressive symptoms within hours and lasting for up to two weeks, even in individuals who are resistant to traditional antidepressants.
"Additional research is needed in this area, but our findings do provide a biological basis for the natural human instinct to self-medicate," Raab-Graham said. "They also define a molecular mechanism that may be a critical contributor to the comorbidity that occurs with alcohol use disorder and major depressive disorder."
Story Source:
Materials provided by Wake Forest Baptist Medical Center. Note: Content may be edited for style and length.
Materials provided by Wake Forest Baptist Medical Center. Note: Content may be edited for style and length.
Journal Reference:
- Sarah A. Wolfe, Emily R. Workman, Chelcie F. Heaney, Farr Niere, Sanjeev Namjoshi, Luisa P. Cacheaux, Sean P. Farris, Michael R. Drew, Boris V. Zemelman, R. Adron Harris, Kimberly F. Raab-Graham. FMRP regulates an ethanol-dependent shift in GABABR function and expression with rapid antidepressant properties. Nature Communications, 2016; 7: 12867 DOI: 10.1038/ncomms12867
Researchers found alcohol follows the same brain pathway as rapid antidepressants.
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."
Alcohol-treated mice showed reduction in depressive-like behaviors
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.
A 'common molecular paradigm' for alcohol and rapid antidepressants
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.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.
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]."
"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."
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