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Chronic adversity dampens dopamine production

November 12, 2019

People exposed to a lifetime of psychosocial adversity may have an impaired ability to produce the dopamine levels needed for coping with acutely stressful situations.

These findings, published today in eLife, may help explain why long-term exposure to psychological trauma and abuse increases the risk of mental illness and addiction.

"We already know that chronic psychosocial adversity can induce vulnerability to mental illnesses such as schizophrenia and depression," explains lead author Dr Michael Bloomfield, Excellence Fellow and leader of the Translational Psychiatry Research Group at University College London, UK. "What we're missing is a precise mechanistic understanding of how this risk is increased."

To address this question, Dr Bloomfield and his colleagues used an imaging technique called positron emission tomography (PET) to compare the production of dopamine in 34 volunteers exposed to an acute stress. Half of the participants had a high lifetime exposure to psychosocial stress, while the other half had low exposure. All of them undertook the Montréal Imaging Stress Task, which involved receiving criticism as they tried to complete mental arithmetic.

Two hours after this stress task, the participants were injected with small amounts of a radioactive tracer that allowed the scientists to view dopamine production in their brains using PET. The scans revealed that in those with low exposure to chronic adversity, dopamine production was proportional to the degree of threat that the person perceived.

In people with high exposure to chronic adversity, however, the perception of threat was exaggerated whilst their production of dopamine was impaired. The researchers found that other physiological responses to stress were also dampened in this group. For example, their blood pressure and cortisol levels did not increase as much as in the low-adversity group in response to stress.

"This study can't prove that chronic psychosocial stress causes mental illness or substance abuse later in life by lowering dopamine levels," Dr Bloomfield cautions. "But we have provided a plausible mechanism for how chronic stress may increase the risk of mental illnesses by altering the brain's dopamine system."

"Further work is now needed to better understand how changes in the dopamine system caused by adversity can lead to vulnerability towards mental illnesses and addiction," adds senior author Oliver Howes, Professor of Molecular Psychiatry at MRC London Institute of Medical Sciences and King's College London, UK.
-end-
Reference

The paper 'The effects of psychosocial stress on dopaminergic function and the acute stress response' can be freely accessed online at https://doi.org/10.7554/eLife.46797. Contents, including text, figures and data, are free to reuse under a CC BY 4.0 license.

Media contact

Emily Packer, Senior Press Officer
eLife
e.packer@elifesciences.org
01223 855373

About eLife

eLife is a non-profit organisation inspired by research funders and led by scientists. Our mission is to help scientists accelerate discovery by operating a platform for research communication that encourages and recognises the most responsible behaviours in science. We publish important research in all areas of the life and biomedical sciences, including Neuroscience, which is selected and evaluated by working scientists and made freely available online without delay. eLife also invests in innovation through open-source tool development to accelerate research communication and discovery. Our work is guided by the communities we serve. eLife is supported by the Howard Hughes Medical Institute, the Max Planck Society, the Wellcome Trust and the Knut and Alice Wallenberg Foundation. Learn more at https://elifesciences.org/about.

To read the latest Neuroscience research published in eLife, visit https://elifesciences.org/subjects/neuroscience.

Full list of funders:

Medical Research Council, National Institute for Health Research, National Institute for Health Research (University College London Hospitals Biomedical Research Centre), Wellcome Trust, University College London, National Institute for Health Research (Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London)

Grant numbers associated with this work:

MC-A656-5QD30, 094849/Z/10/Z

eLife

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