Chloe C Boyle1, Annette L Stanton2, Naomi I Eisenberger3, Teresa E Seeman4, Julienne E Bower2. 1. Norman Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Behavior, University of California, Los Angeles, CA 90095, United States. Electronic address: ccboyle@ucla.edu. 2. Norman Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Behavior, University of California, Los Angeles, CA 90095, United States; Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, CA 90095, United States; Department of Psychology, University of California, Los Angeles, CA 90095, United States. 3. Department of Psychology, University of California, Los Angeles, CA 90095, United States. 4. Geffen School of Medicine, University of California, Los Angeles, CA 90095, United States.
Abstract
BACKGROUND: Anhedonia, or loss of interest or pleasure, is a feature of depression and transdiagnostic construct in psychopathology. Theory and compelling evidence from preclinical models implicates stress-induced inflammation as a psychobiological pathway to anhedonic behavior; however, this pathway has not been tested in human models. Further, although anhedonia may reflect dysregulation in multiple dimensions of reward, the extent to which stress-induced inflammation alters these dimensions is unclear. Thus, the current experimental study used a standardized laboratory stressor task to elicit an inflammatory response and evaluate effects of stress-induced inflammation on multiple behavioral indices of reward processing. METHODS:Healthy young women (age 18-25) completedbehavioral reward tasks assessing reward learning, motivation, and sensitivity and were randomized to undergo an acute psychosocial stressor (n = 37) or a no-stress active control (n = 17). Tasks were re-administered 90-120 min post-stress to coincide with the peak of the stress-induced inflammatory response. Blood samples were collected for assessment of the pro-inflammatory cytokine interleukin-6 (IL-6) at baseline and 90 and 120 min post stressor. RESULTS: Stress-induced IL-6 was associated with increased response bias during reward learning and increased motivation when probability of receiving a reward was low. Sensitivity to reward in the context of a motivation task was not altered in association with stress-induced IL-6. CONCLUSIONS: Contrary to hypotheses, mild increases in IL-6 following acute stress were associated with increased reward responsiveness during reward learning and selective increases in motivation. Results contribute to an emerging and nuanced literature linking inflammation to reward processing, and demonstrate that behavioral effects of stress-induced inflammation may be detected in the laboratory setting. CLINICAL TRIAL REGISTRATION: NCT03828604.
RCT Entities:
BACKGROUND:Anhedonia, or loss of interest or pleasure, is a feature of depression and transdiagnostic construct in psychopathology. Theory and compelling evidence from preclinical models implicates stress-induced inflammation as a psychobiological pathway to anhedonic behavior; however, this pathway has not been tested in human models. Further, although anhedonia may reflect dysregulation in multiple dimensions of reward, the extent to which stress-induced inflammation alters these dimensions is unclear. Thus, the current experimental study used a standardized laboratory stressor task to elicit an inflammatory response and evaluate effects of stress-induced inflammation on multiple behavioral indices of reward processing. METHODS: Healthy young women (age 18-25) completed behavioral reward tasks assessing reward learning, motivation, and sensitivity and were randomized to undergo an acute psychosocial stressor (n = 37) or a no-stress active control (n = 17). Tasks were re-administered 90-120 min post-stress to coincide with the peak of the stress-induced inflammatory response. Blood samples were collected for assessment of the pro-inflammatory cytokine interleukin-6 (IL-6) at baseline and 90 and 120 min post stressor. RESULTS:Stress-induced IL-6 was associated with increased response bias during reward learning and increased motivation when probability of receiving a reward was low. Sensitivity to reward in the context of a motivation task was not altered in association with stress-induced IL-6. CONCLUSIONS: Contrary to hypotheses, mild increases in IL-6 following acute stress were associated with increased reward responsiveness during reward learning and selective increases in motivation. Results contribute to an emerging and nuanced literature linking inflammation to reward processing, and demonstrate that behavioral effects of stress-induced inflammation may be detected in the laboratory setting. CLINICAL TRIAL REGISTRATION: NCT03828604.
Authors: George M Slavich; Baldwin M Way; Naomi I Eisenberger; Shelley E Taylor Journal: Proc Natl Acad Sci U S A Date: 2010-08-02 Impact factor: 11.205
Authors: J D Johnson; J Campisi; C M Sharkey; S L Kennedy; M Nickerson; B N Greenwood; M Fleshner Journal: Neuroscience Date: 2005-09-13 Impact factor: 3.590
Authors: I Goshen; T Kreisel; O Ben-Menachem-Zidon; T Licht; J Weidenfeld; T Ben-Hur; R Yirmiya Journal: Mol Psychiatry Date: 2007-08-14 Impact factor: 15.992
Authors: Melissa A Rosenkranz; Stephane Esnault; Lauren Gresham; Richard J Davidson; Bradley T Christian; Nizar N Jarjour; William W Busse Journal: Biol Psychol Date: 2021-11-17 Impact factor: 3.111
Authors: Iris Ka-Yi Chat; Robin Nusslock; Daniel P Moriarity; Corinne P Bart; Naoise Mac Giollabhui; Katherine S F Damme; Ann L Carroll; Gregory E Miller; Lauren B Alloy Journal: Brain Behav Immun Date: 2021-03-09 Impact factor: 7.217