Background Stress is widely known to alter behavioral responses to rewards and punishments. It is believed that stress may precipitate these changes through modulation of corticostriatal circuitry involved in reinforcement learning and motivation, although the intervening mechanisms remain unclear. One candidate is inflammation, which can rapidly increase following stress, and can disrupt dopamine-dependent reward pathways. Methods Here, in a sample of 88 healthy female participants, we first assessed the effect of an acute laboratory stress paradigm on levels of plasma interleukin-6 (IL-6), a cytokine known to be both responsive to stress and elevated in depression. In a second laboratory session, we examined the effects of a second laboratory stress paradigm on reward prediction error (RPE) signaling in the ventral striatum. Results We show that individual differences in stress-induced increases in IL-6 (session 1) were associated with decreased ventral striatal RPE signaling during reinforcement learning (session 2), though there was no main effect of stress on RPE. Further, changes in IL-6 following stress predicted intra-individual variability in perceived stress during a 4-month follow-up period. Conclusions Taken together, these data identify a novel link between IL-6 and striatal reward prediction errors during reinforcement learning in the context of acute psychological stress, as well as future appraisal of stressful life events.
Background Although cognitive theories of depression have postulated enhanced processing of negatively valenced information, previous EEG studies have shown both increased and reduced sensitivity for negative performance feedback in MDD. To reconcile these paradoxical findings, it has been speculated that sensitivity for negative feedback is potentiated in moderate MDD but reduced in highly anhedonic subjects. The goal of this study was to test this hypothesis by analyzing the feedback-related negativity (FRN), frontomedial theta power (FMT), and source-localized anterior midcingulate cortex (aMCC) activity after negative feedback. Methods Fourteen unmedicated participants with MDD and 15 control participants performed a reinforcement learning task while 128-channel EEG was recorded. FRN, FMT and LORETA source-localized aMCC activity after negative and positive feedback were compared between groups. Results The MDD group showed higher FRN amplitudes and aMCC activation to negative feedback than controls. Moreover, aMCC activation to negative feedback was inversely related to self-reported anhedonia. In contrast, self-reported anxiety correlated with feedback-evoked frontomedial theta (FMT) within the depression group. Conclusions The present findings suggest that, among depressed and anxious individuals, enhanced processing of negative feedback occurs relatively early in the information processing stream. These results extend prior work and indicate that although moderate depression is associated with elevated sensitivity for negative feedback, high levels of anhedonia may attenuate this effect.
Within the rough ground that is the field of education there is a complex web of ethical obligations: to prepare our students for their future work; to be ethical as educators in our conduct and teaching; to the ethical principles embedded in the contexts in which we work; and given the Southern context of this work, the ethical obligations we have to this land and its First Peoples. We put out a call to colleagues whose work has been concerned with the pedagogies of professional ethics, the ethical burdens of institutional injustice, and the application of ethical theory to education's applied fields. In the responses we received it can be seen that ethical concerns in education are broad ranging, covering terrain varying from the preparation of preservice teachers, ethics in higher education, early childhood and care, educational leadership, relational and communicative ethics. Perhaps it could also be argued that this paper demonstrates Gibbon's observation that 'Assumptions about the particularity of this time as new and ripe with opportunity to make a difference through philosophy of education are not new and there's much tolearnfrom the persistence of wanting to imagine that they are ' (in Peters et al., 2020, p. 17). However, while the field of ethics is perennially con-cerned with human relations and pedagogical interventions to improve these, the responses collected here show that educational ethics is far from static. Educational ethics is a field that continues to develop in response to changing contexts.
Major depressive disorder (MDD) and nicotine dependence are highly comorbid, with studies showing that ~50% of individuals with MDD smoke. The link between these disorders persists even after the clinical symptoms of depression subside, as indicated by high levels of nicotine dependence among individuals with remitted depression (rMDD). Recent evidence indicates that individuals with rMDD show blunted responses to reward as measured by a probabilistic reward task (PRT), which assesses the ability to modify behavior as a function of reward history. Given nicotine's ability to enhance reward responsiveness, individuals with rMDD might smoke to address this persistent reward deficit. However, it is unclear whether smokers with rMDD show enhanced reward responsiveness relative to rMDD individuals who do not smoke. To test this hypothesis, we evaluated reward responsiveness on the PRT in four groups (N=198): individuals with and without rMDD who were or were not nicotine dependent. As hypothesized, rMDD nonsmokers had lower reward responsiveness relative to both control nonsmokers and rMDD smokers; conversely, smokers with rMDD showed behavioral patterns comparable to those without a history of depression. Given nicotine's ability to enhance reward sensitivity, it is possible that nicotine normalizes the otherwise blunted reward responsiveness in individuals with rMDD. Therapies aimed at enhancing this reward-based deficit may be beneficial in the treatment of both nicotine dependence and MDD.
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