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. 2019 Nov 12:8:e46797.
doi: 10.7554/eLife.46797.

The effects of psychosocial stress on dopaminergic function and the acute stress response

Michael Ap Bloomfield  1   2   3   4   5   6   7 , Robert A McCutcheon  1   3 , Matthew Kempton  3 , Tom P Freeman  2   4   8 , Oliver Howes  1   3
Affiliations

The effects of psychosocial stress on dopaminergic function and the acute stress response

Michael Ap Bloomfield et al. Elife. .

Abstract

Chronic psychosocial adversity induces vulnerability to mental illnesses. Animal studies demonstrate that this may be mediated by dopaminergic dysfunction. We therefore investigated whether long-term exposure to psychosocial adversity was associated with dopamine dysfunction and its relationship to psychological and physiological responses to acute stress. Using 3,4-dihydroxy-6-[18F]-fluoro-l-phenylalanine ([18F]-DOPA) positron emission tomography (PET), we compared dopamine synthesis capacity in n = 17 human participants with high cumulative exposure to psychosocial adversity with n = 17 age- and sex-matched participants with low cumulative exposure. The PET scan took place 2 hr after the induction of acute psychosocial stress using the Montréal Imaging Stress Task to induce acute psychosocial stress. We found that dopamine synthesis correlated with subjective threat and physiological response to acute psychosocial stress in the low exposure group. Long-term exposure to psychosocial adversity was associated with dampened striatal dopaminergic function (p=0.03, d = 0.80) and that psychosocial adversity blunted physiological yet potentiated subjective responses to acute psychosocial stress. Future studies should investigate the roles of these changes in vulnerability to mental illnesses.

Keywords: PET; adversity; human; imaging; neuroscience; psychosocial; stress; threat.

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Conflict of interest statement

MB, RM, MK, TF No competing interests declared, OH Professor Howes has received investigator-initiated research funding from and/or participated in advisory/speaker meetings organised by Astra-Zeneca, Autifony, BMS, Eli Lilly, Heptares, Jansenn, Lundbeck, Lyden-Delta, Otsuka, Servier, Sunovion, Rand and Roche. Neither Professor Howes nor his family have been employed by or have holdings/a financial stake in any biomedical company.

Figures

Figure 1.
Figure 1.. Striatal dopamine synthesis capacity in Low Adversity (LA, n = 17) and High Adversity participants (HA, n = 17).
Dopamine synthesis capacity was significantly reduced in HA compared with LA (t32 = 2.27, p=0.03). Error bars indicate standard errors.
Figure 2.
Figure 2.. The High Adversity group showed a heightened subjective response and a blunted physiological response.
Panel A shows subjective Threatened responses; Panels B (Cortisol) and C (Mean Arterial Blood Pressure) show physiological response. Data show mean (+ /- SEM).
Figure 3.
Figure 3.. Correlations between striatal dopamine synthesis capacity and acute response to psychosocial stress.
(A) Whole striatal dopamine synthesis capacity was positively correlated with stress-induced threat in the Low Adversity group (r = 0.73, p=0.001) but not the High Adversity group (r = −0.03, p=0.934). (B). Whole striatal dopamine synthesis capacity was negatively correlated with stress-induced threat and mean arterial blood pressure in the Low Adversity group (r = −0.62, p=0.013) but not the High Adversity group (r = 0.23, p=0.395). Extreme bivariate outliers have been removed from the figures.
Figure 4.
Figure 4.. Experimental procedures.
MIST, Montreal Imaging Stress Test; MAP, Mean Arterial Blood Pressure; VAS, visual analogue scale.
See this image and copyright information in PMC

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