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Trait rumination and response to negative evaluative lab-induced stress: neuroendocrine, affective, and cognitive outcomes.

ABSTRACT: Theoretical models of depression posit that, under stress, elevated trait rumination predicts more pronounced or prolonged negative affective and neuroendocrine responses, and that trait rumination hampers removing irrelevant negative information from working memory. We examined several gaps regarding these models in the context of lab-induced stress. Non-depressed undergraduates completed a rumination questionnaire and either a negative-evaluative Trier Social Stress Test (n?=?55) or a non-evaluative control condition (n?=?69), followed by a modified Sternberg affective working memory task assessing the extent to which irrelevant negative information can be emptied from working memory. We measured shame, negative and positive affect, and salivary cortisol four times. Multilevel growth curve models showed rumination and stress interactively predicted cortisol reactivity; however, opposite predictions, greater rumination was associated with blunted cortisol reactivity to stress. Elevated trait rumination interacted with stress to predict augmented shame reactivity. Rumination and stress did not significantly interact to predict working memory performance, but under control conditions, rumination predicted greater difficulty updating working memory. Results support a vulnerability-stress model of trait rumination with heightened shame reactivity and cortisol dysregulation rather than hyper-reactivity in non-depressed emerging adults, but we cannot provide evidence that working memory processes are critical immediately following acute stress.

SUBMITTER: Vrshek-Schallhorn S

PROVIDER: S-EPMC6174001 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature

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Trait rumination and response to negative evaluative lab-induced stress: neuroendocrine, affective, and cognitive outcomes.

Vrshek-Schallhorn Suzanne S Velkoff Elizabeth A EA Zinbarg Richard E RE

Cognition & emotion 20180406 3

Theoretical models of depression posit that, under stress, elevated trait rumination predicts more pronounced or prolonged negative affective and neuroendocrine responses, and that trait rumination hampers removing irrelevant negative information from working memory. We examined several gaps regarding these models in the context of lab-induced stress. Non-depressed undergraduates completed a rumination questionnaire and either a negative-evaluative Trier Social Stress Test (n = 55) or a non-eval ...[more]

PMID: 29623753

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Project description:An adverse environment in early life is often associated with dysregulation of the hypothalamo-pituitary-adrenal (HPA) axis and higher rates of mood disorders in adulthood. In rats, exposure to social stress during pregnancy results in hyperactive HPA axis responses to stress in the adult offspring and heightened anxiety behavior in the males, but not the females. Here we tested whether, without further intervention, the effects of prenatal stress (PNS) in the first filial generation (F1) are transmitted to the F2 generation via the maternal line. F1 control and PNS female rats were mated with control males and housed under non-stress conditions throughout pregnancy. HPA axis responses to acute stress, anxiety- and depressive-like behavior were assessed in the adult F2 offspring. ACTH and corticosterone responses to an acute stressor were markedly enhanced in F2 PNS females compared with controls. This was associated with greater corticotropin releasing hormone (Crh) mRNA expression in the paraventricular nucleus and reduced hippocampal glucocorticoid (Gr) and mineralocorticoid receptor (Mr) mRNA expression. Conversely, in the F2 PNS males, HPA axis responses to acute stress were attenuated and hippocampal Gr mRNA expression was greater compared with controls. F2 PNS males exhibited heightened anxiety-like behavior (light-dark box and elevated plus maze) compared with F2 control males. Anxiety-like behavior did not differ between F2 control and PNS females during metestrus/diestrus, however at proestrus/estrus, F2 control females displayed a reduction in anxiety-like behavior, but this effect was not observed in the F2 PNS females. Heightened anxiety in the F2 PNS males was associated with greater Crh mRNA expression in the central nucleus of the amygdala compared with controls. Moreover, Crh receptor-1 (Crhr1) mRNA expression was significantly increased, whereas Crhr2 mRNA was significantly decreased in discrete regions of the amygdala in F2 PNS males compared with controls, with no differences in the F2 females. No differences in depressive-like behavior (sucrose preference or forced swim test) were observed in either sex. In conclusion, the effects of maternal stress during pregnancy on HPA axis regulation and anxiety-like behavior can be transmitted to future generations in a sex-dependent manner. These data have implications for human neuropsychiatric disorders with developmental origins.

Dataset Information

Trait rumination and response to negative evaluative lab-induced stress: neuroendocrine, affective, and cognitive outcomes.

Publications

Trait rumination and response to negative evaluative lab-induced stress: neuroendocrine, affective, and cognitive outcomes.

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