Stress-related Gene (MKP-1 or MKP1), Depression, and Heat Stress


Duman’s team did whole genome scans on tissue samples from 21 deceased individuals who had been diagnosed with depression and compared gene expression levels to those of 18 individuals who had not been diagnosed with depression. They found that one gene called MKP-1 was increased more than two-fold in the brain tissues of depressed individuals.

This was particularly exciting, say the researchers, because the gene inactivates a molecular pathway crucial to the survival and function of neurons and its impairment has been implicated in depression as well as other disorders. Duman’s team also found that when the MKP-1 gene is knocked out in mice, the mice become resilient to stress. When the gene is activated, mice exhibit symptoms that mimic depression.

The finding that a negative regulator of a key neuronal signaling pathway is increased in depression also identifies MKP-1 as a potential target for a novel class of therapeutic agents, particularly for treatment resistant depression. (via.)

Interesting tidbits from elsewhere:


Heightened immune response in socially anxious


Everyone experiences social stress, whether it is nervousness over a job interview, difficulty meeting people at parties, or angst over giving a speech. In a new report, UCLA researchers have discovered that how your brain responds to social stressors can influence the body’s immune system in ways that may negatively affect health.

Lead author George Slavich, a postdoctoral fellow at the UCLA Cousins Center for Psychoneuroimmunology, and senior author Shelley Taylor, a UCLA professor of psychology, show that individuals who exhibit greater neural sensitivity to social rejection also exhibit greater increases in inflammatory activity to social stress. [...]

The researchers recruited 124 individuals — 54 men and 70 women — and put them into two awkward social situations. First, in the lab, the volunteers completed the Trier Social Stress Test (TSST), which involves preparing and delivering an impromptu speech and performing difficult mental arithmetic, both in front of a socially rejecting panel of raters wearing white lab coats. Mouth swabs were taken before and after the public-speaking tasks to test for changes in two key biomarkers of inflammatory activity — a receptor for tumor necrosis factor-? (sTNF?RII) and interleukin-6 (IL-6).

In a second session, 31 of the participants received an MRI brain scan while playing a computerized game of catch with what they believed were two other real people. The researchers focused on two areas of the brain known to respond to social stress — the dorsal anterior cingulate cortex (dACC) and the anterior insula.

At first, the game was between all three “players.” Halfway through the game, however, the research subject was excluded, leading to an experience of social rejection. The researchers then examined how differences in neural activity during social rejection correlated with differences in inflammatory responses to the TSST.

Their results showed that individuals who exhibited greater neural activity in the dorsal anterior cingulate cortex and anterior insula during social rejection in the brain scanner also exhibited greater increases in inflammatory activity when exposed to acute social stress in the lab.

“This is further evidence of how closely our mind and body are connected,” Slavich said. “We have known for a long time that social stress can ‘get under the skin’ to increase risk for disease, but it’s been unclear exactly how these effects occur. To our knowledge, this study is the first to identify the neurocognitive pathways that might be involved in inflammatory responses to acute social stress.” [...]

One critical question raised by the present findings is why neural sensitivity to social rejection would cause an increase in inflammation. There are several possible reasons, the authors note. For one, since physical threats have historically gone hand in hand with social threat or rejection, inflammation may be triggered in anticipation of a physical injury. Inflammatory cytokines — proteins that regulate the immune system — are released in response to impending (or actual) physical assault because they accelerate wound-healing and reduce the risk of infection.

via.

This may also be of interest: Tylenol (acetaminophen) eases social anxiety.