14 DAY TRIAL // In a new scientific investigation conducted on unsuspecting lab mice, researchers demonstrated for the first time ever that drug abuse can set the stage for the development of stress-related diseases in the human brain, such as for example depression.
Until now, the opposite was demonstrated several times over. Researchers widely agree that depression can lead to dangerous behaviors, such as becoming addicted to cigarettes, coffee, alcohol or drugs.
However, it was only recently that scientists were able to establish for a fact that the opposite is also true. For this particular research, the team used cocaine to make mice addicted to drugs. The more cocaine the rodents got, the more depressed they became.
The group noticed a severe increase in depression-related symptoms among the animals that received the largest amounts of the drug. Using complex study techniques, the Mount Sinai School of Medicine team was able to identify the neural pathway that underlies this vulnerability.
These new discoveries could potentially be used for the development of novel treatment and therapies for depression, post-traumatic stress disorder (PTSD) and other mental illnesses whose development is heavily dictated by stres..
MSSM research scientist Dr. Eric Nestler was the senior author of the new study. A paper detailing the findings appears in the latest issue of the esteemed medical journal Neuron, PsychCentral reports.
“Clinical evidence shows that substance abuse can increase an individual’s risk for a mood disorder,” Dr. Nestler argues. He and his team proposed that using drugs in fact triggered altered responses to stress in the brain of test mice.
The tiny rodents were used because their brain structure is surprisingly similar to our own in this regard. As such, they can be used as research proxies for the human brain. The team focused the study on the prominent chromosomal modification called histone H3 lysine 9 dimethylation (H3K9me2).
What they wanted to surmise was whether it played a role in aiding cocaine addiction clear a path for depression-like symptoms in the brain's natural defenses. The team learned that the modification was indeed a part of this pathway.
“Together, our results provide fundamentally novel insight into how prior exposure to a drug of abuse enhances vulnerability to depression and other stress-related disorders,” Dr. Nestler explains.
“Identifying such common regulatory mechanisms may aid in the development of new therapies for addiction and depression,” he concludes.