Despite the fact that there are therapies available for depression, many people find them useless at times. Furthermore, women are more prone than men to suffer from depression, although the reason for this disparity is unknown. This can make addressing their problems more difficult at times.
The study’s findings were published in the journal Biological Psychiatry this month. Researchers from the University of California, Davis collaborated with experts from Mt. Sinai Hospital, Princeton University, and Laval University in Quebec to try to understand how depression affects a specific area of the brain, the nucleus accumbens.
The nucleus accumbens is involved in motivation, responding to pleasurable events, and social relationships, all of which are impacted by depression.
Previous research in the nucleus accumbens found that distinct genes were switched on or off in women with depression but not in males. These modifications might have generated depression symptoms, or the experience of being depressed could have changed the brain. To distinguish between these options, the researchers analysed mice that had had unfavourable social interactions, which cause females to exhibit more depression-related behaviour than males.
“These high-throughput studies are extremely useful in understanding the long-term consequences of stress on the brain. Negative social interactions in our rodent model altered gene expression patterns in female mice, mirroring patterns reported in women with depression “Alexia Williams, a PhD researcher and recent UC Davis graduate who conceived and directed these investigations, expressed her excitement. “This is interesting because women have been understudied in this subject, and this discovery has allowed me to focus my attention on the significance of these facts for women’s health.”
“Comparative transcriptional studies in the nucleus accumbens identify RGS2 as a significant modulator of depression-related behaviour,” according to the research. Following the discovery of comparable chemical alterations in the brains of mice and humans, researchers sought to tweak one gene, regulator of g protein signaling-2, or Rgs2.
This gene modulates the production of a protein that regulates neurotransmitter receptors, which are targeted by antidepressants like Prozac and Zoloft. “We were curious to see whether increasing Rgs2 in the nucleus accumbens could reduce depression-related behaviours because less stable versions of the Rgs2 protein are associated with an increased risk of depression in humans,” said Brian Trainor, UC Davis professor of psychology and senior author on the study. He is also a member of the Center for Neuroscience and the director of the Behavioral Neuroendocrinology Lab at UC Davis.
When the researchers experimentally raised Rgs2 protein in the mice’s nucleus accumbens, they effectively reversed the effects of stress on these female mice, finding that social approach and preferences for favourite meals increased to levels seen in females who had not been stressed.
“These findings point to a biological mechanism that contributes to the lack of drive commonly reported in depressed individuals.” “Reduced function of proteins like Rgs2 may contribute to difficult-to-treat symptoms in people suffering from mental diseases,” Williams added.
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According to the researchers, findings from basic science studies like this one might help lead the development of pharmacotherapies to successfully treat people suffering from depression.
“Our aim is that by conducting research like this, which focus on clarifying processes underlying particular symptoms of complicated mental diseases,” Williams added.
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