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Effects of stress-induced inflammation on reward processing in healthy young women.
Boyle, Chloe C; Stanton, Annette L; Eisenberger, Naomi I; Seeman, Teresa E; Bower, Julienne E.
Afiliación
  • Boyle CC; 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.
  • Stanton AL; 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 Psycholog
  • Eisenberger NI; Department of Psychology, University of California, Los Angeles, CA 90095, United States.
  • Seeman TE; Geffen School of Medicine, University of California, Los Angeles, CA 90095, United States.
  • Bower JE; 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 Psycholog
Brain Behav Immun ; 83: 126-134, 2020 01.
Article en En | MEDLINE | ID: mdl-31580931
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) 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.
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Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Recompensa / Estrés Psicológico / Inflamación / Motivación Tipo de estudio: Clinical_trials / Prognostic_studies Límite: Adolescent / Adult / Female / Humans Idioma: En Revista: Brain Behav Immun Asunto de la revista: ALERGIA E IMUNOLOGIA / CEREBRO / PSICOFISIOLOGIA Año: 2020 Tipo del documento: Article

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Recompensa / Estrés Psicológico / Inflamación / Motivación Tipo de estudio: Clinical_trials / Prognostic_studies Límite: Adolescent / Adult / Female / Humans Idioma: En Revista: Brain Behav Immun Asunto de la revista: ALERGIA E IMUNOLOGIA / CEREBRO / PSICOFISIOLOGIA Año: 2020 Tipo del documento: Article