A mechanistic account of serotonin's impact on mood.
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ABSTRACT:
SUBMITTER: Michely J
PROVIDER: S-EPMC7214430 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Implicit social biases play a critical role in shaping our attitudes towards other people. Such biases are thought to arise, in part, from a comparison between features of one's own self-image and those of another agent, a process known as 'bodily resonance'. Recent data have demonstrated that implicit bias can be remarkably plastic, being modulated by brief immersive virtual reality experiences that place participants in a virtual body with features of an out-group member. Here, we provide a mechanistic account of bodily resonance and implicit bias in terms of a putative self-image network that encodes associations between different features of an agent. When subsequently perceiving another agent, the output of this self-image network is proportional to the overlap between their respective features, providing an index of bodily resonance. By combining the self-image network with a drift diffusion model of decision making, we simulate performance on the implicit association test (IAT) and show that the model captures the ubiquitous implicit bias towards in-group members. We subsequently demonstrate that this implicit bias can be modulated by a simulated illusory body ownership experience, consistent with empirical data; and that the magnitude and plasticity of implicit bias correlates with self-esteem. Hence, we provide a simple mechanistic account of bodily resonance and implicit bias which could contribute to the development of interventions for reducing the negative evaluation of social out-groups.
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Project description:The influence of mood on choices is a well-established but poorly understood phenomenon. Here, we suggest a three-fold neuro-computational account: (1) the integration of positive and negative events over time induce mood fluctuations, (2) which are underpinned by variations in the baseline activities of critical brain valuation regions, (3) which in turn modulate the relative weights assigned to key dimensions of choice options. We validate this model in healthy participants, using feedback in a quiz task to induce mood fluctuations, and a choice task (accepting vs. declining a motor challenge) to reveal their effects. Using fMRI, we demonstrate the pivotal role of the ventromedial prefrontal cortex and anterior insula, in which baseline activities respectively increase and decrease with theoretical mood level and respectively enhance the weighting of potential gains and losses during decision making. The same mechanisms might explain how decisions are biased in mood disorders at longer timescales.
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Project description:To make decisions based on the value of different options, we often have to combine different sources of probabilistic evidence. For example, when shopping for strawberries on a fruit stand, one uses their color and size to infer-with some uncertainty-which strawberries taste best. Despite much progress in understanding the neural underpinnings of value-based decision making in humans, it remains unclear how the brain represents different sources of probabilistic evidence and how they are used to compute value signals needed to drive the decision. Here, we use a visual probabilistic categorization task to show that regions in ventral temporal cortex encode probabilistic evidence for different decision alternatives, while ventromedial prefrontal cortex integrates information from these regions into a value signal using a difference-based comparator operation.
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Project description:ObjectiveThe need for measuring emotional functioning in patients with chronic pain was recognized decades ago. The Initiative on Methods, Measures, and Pain Assessment in Clinical Trials (IMMPACT) proposed the Profile of Mood States for this purpose. However, to date, its factor structure has not been confirmed in these patients.MethodsWe set out to use confirmatory factor analysis to test the theoretical structure of seven factors: Tension-Anxiety, Depression-Dejection, Anger-Hostility, Vigor-Activity, Fatigue-Inertia, Confusion-Bewilderment, and Friendliness.ParticipantsThe sample consisted of 588 Spanish adult patients with chronic pain.ResultsThe original structure could not be verified according to the obtained fit indices (e.g., root-mean-square error of approximation = 0.11). For this reason, we carried out a second study that relied on exploratory factor analysis to evaluate the structure in half of the cases and confirmatory factor analysis to validate it in the other half. The factor structure detected in the exploratory factor analysis was not satisfactory, nor could it be validated with confirmatory factor analysis (e.g., normed fit index between 0.54 and 0.56).ConclusionsThe factor structure of the Profile of Mood States could not be satisfactorily confirmed. Consequently, other mood measures and shorter, optimized versions of the POMS are discussed as possible alternatives.
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Project description:The aim of this study was to investigate whether baseline mood and/or mood while drinking have an impact on alcohol hangover severity. A survey was held among N = 331 young adults (mean age = 23.6 years, range = 18-35 years). Demographics, alcohol consumption, subjective intoxication, and hangover severity were assessed for the past three days. In addition, mood (baseline, while drinking, and during hangover) was also assessed. N = 143 participants reported to be hungover on the day of assessment, N = 122 participants reported to have been hungover the previous day ('yesterday'), and N = 87 participants reported to have been hungover two days before the assessment ('2 days ago'). The analyses revealed that baseline mood and mood while drinking had no relevant effect on the amount of consumed alcohol and did not significantly contribute to hangover severity. However, hangover severity was associated with significantly increased negative affect, particularly with higher levels of subjective stress on the day of the hangover.
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Project description:Gulf War Illness is a chronic multisystem disorder affecting approximately a third of the Veterans of the Gulf War, manifesting with physical and mental health symptoms such as cognitive impairment, neurological abnormalities, and dysregulation of mood. Among the leading theories into the etiology of this multisystem disorder is environmental exposure to the various neurotoxins encountered in the Gulf Theatre, including organophosphates, nerve agents, pyridostigmine bromide, smoke from oil well fires, and depleted uranium. The relationship of toxin exposure and the pathogenesis of Gulf War Illness converges on the innate immune system: a nonspecific form of immunity ubiquitous in nature that acts to respond to both exogenous and endogenous insults. Activation of the innate immune system results in inflammation mediated by the release of cytokines. Cytokine mediated neuroinflammation has been demonstrated in a number of psychiatric conditions and may help explain the larger than expected population of Gulf War Veterans afflicted with a mood disorder. Several of the environmental toxins encountered by soldiers during the first Gulf War have been shown to cause upregulation of inflammatory mediators after chronic exposure, even at low levels. This act of inflammatory priming, by which repeated exposure to chronic subthreshold insults elicits robust responses, even after an extended period of latency, is integral in the connection of Gulf War Illness and comorbid mood disorders. Further developing the understanding of the relationship between environmental toxin exposure, innate immune activation, and pathogenesis of disease in the Gulf War Veterans population, may yield novel therapeutic targets, and a greater understanding of disease pathology and subsequently prevention.
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Project description:Previous research has found that funding disparities are driven by applications' final impact scores and that only a portion of the black/white funding gap can be explained by bibliometrics and topic choice. Using National Institutes of Health R01 applications for council years 2014-2016, we examine assigned reviewers' preliminary overall impact and criterion scores to evaluate whether racial disparities in impact scores can be explained by application and applicant characteristics. We hypothesize that differences in commensuration-the process of combining criterion scores into overall impact scores-disadvantage black applicants. Using multilevel models and matching on key variables including career stage, gender, and area of science, we find little evidence for racial disparities emerging in the process of combining preliminary criterion scores into preliminary overall impact scores. Instead, preliminary criterion scores fully account for racial disparities-yet do not explain all of the variability-in preliminary overall impact scores.
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Project description:Introduction: In Europe, women can expect to live on average 82 years and men 75 years. Forecasting how life expectancy will develop in the future is essential for society. Most forecasts rely on a mechanical extrapolation of past mortality trends, which leads to unreliable outcomes because of temporal fluctuations in the past trends due to lifestyle 'epidemics'. Methods: We project life expectancy for 18 European countries by taking into account the impact of smoking, obesity, and alcohol on mortality, and the mortality experiences of forerunner populations. Results: We project that life expectancy in these 18 countries will increase from, on average, 83.4 years for women and 78.3 years for men in 2014 to 92.8 years for women and 90.5 years for men in 2065. Compared to others (Lee-Carter, Eurostat, United Nations), we project higher future life expectancy values and more realistic differences between countries and sexes. Conclusions: Our results imply longer individual lifespans, and more elderly in society. Funding: Netherlands Organisation for Scientific Research (NWO) (grant no. 452-13-001).
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Project description:The CARD11 scaffold controls antigen receptor signaling to NF-κB, JNK, and mTOR. Three classes of germline mutations in CARD11 cause Primary Immunodeficiency, including homozygous loss-of-function (LOF) mutations in CARD11 deficiency, heterozygous gain-of-function (GOF) mutations in BENTA disease, and heterozygous dominant-negative LOF mutations in CADINS. Here, we characterize LOF CARD11 mutants with a range of dominant-negative activities to identify the mechanistic properties that cause these variants to exert dominant effects when heterozygous. We find that strong dominant negatives can poison signaling from mixed wild-type:mutant oligomers at two steps in the CARD11 signaling cycle, at the Opening Step and at the Cofactor Association Step. Our findings provide evidence that CARD11 oligomer subunits cooperate in at least two steps during antigen receptor signaling and reveal how different LOF mutations in the same oligomeric signaling hub may cause disease with different inheritance patterns.
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Project description:BACKGROUND:Maladaptive responses to negative affective stimuli are pervasive, including clinically ill and healthy people, and men and women respond differently at neural and hormonal levels. Inspired by the Research Domain Criteria initiative, we used a transdiagnostic approach to investigate the impact of sex and dysphoric mood on neural-hormonal responses to negative affective stimuli. METHODS:Participants included 99 individuals with major depressive disorder, psychosis and healthy controls. Functional magnetic resonance imaging (fMRI) was complemented with real-time acquisition of hypothalamo-pituitary-adrenal (HPA) and -gonadal (HPG) hormones. fMRI data were analyzed in SPM8 and task-related connectivity was assessed using generalized psychophysiological interaction. RESULTS:Across all participants, elevated cortisol response predicted lower brain activity in orbitofrontal cortex and hypothalamus-amygdala connectivity. In those with worse dysphoric mood, elevated cortisol response predicted lower activity in hypothalamus and hippocampus. In women, elevated cortisol response was associated with lower activity in medial prefrontal cortex and low hypothalamo-hippocampal connectivity. In women with high dysphoric mood, elevated cortisol response was associated with low hypothalamo-hippocampal connectivity. There were no interactions with diagnosis or medication. LIMITATIONS:There was limited power to correct for multiple comparisons across total number of ROIs and connectivity targets; cortisol responses were relatively low. CONCLUSIONS:We conclude that the pathophysiology in neural-hormonal responses to negative affective stimuli is shared across healthy and clinical populations and varies as a function of sex and dysphoric mood. Our findings may contribute to the development of hormonal adjunctive therapeutics that are sex-dependent, underscoring the importance of one's sex to precision medicine.
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