The neural basis of smile authenticity judgments and the potential modulatory role of the oxytocin receptor gene (OXTR).

Accurate perception of genuine vs. posed smiles is crucial for successful social navigation in humans. While people vary in their ability to assess the authenticity of smiles, little is known about the specific biological mechanisms underlying this variation. We investigated the neural substrates of smile authenticity judgments using functional magnetic resonance imaging (fMRI). We also tested a preliminary hypothesis that a common polymorphism in the oxytocin receptor gene (OXTR) rs53576 would modulate the behavioral and neural indices of accurate smile authenticity judgments. A total of 185 healthy adult participants (Neuroimaging arm: N = 44, Behavioral arm: N = 141) determined the authenticity of dynamic facial expressions of genuine and posed smiles either with or without fMRI scanning. Correctly identified genuine vs. posed smiles activated brain areas involved with reward processing, facial mimicry, and mentalizing. Activation within the inferior frontal gyrus and dorsomedial prefrontal cortex correlated with individual differences in sensitivity (d') and response criterion (C), respectively. Our exploratory genetic analysis revealed that rs53576 G homozygotes in the neuroimaging arm had a stronger tendency to judge posed smiles as genuine than did A allele carriers and showed decreased activation in the medial prefrontal cortex when viewing genuine vs. posed smiles. Yet, OXTR rs53576 did not modulate task performance in the behavioral arm, which calls for further studies to evaluate the legitimacy of this result. Our findings extend previous literature on the biological foundations of smile authenticity judgments, particularly emphasizing the involvement of brain regions implicated in reward, facial mimicry, and mentalizing.

Blood levels of T-Cell Receptor Excision Circles (TRECs) provide an index of exposure to traumatic stress in mice and humans.

Exposure to stress triggers biological changes throughout the body. Accumulating evidence indicates that alterations in immune system function are associated with the development of stress-associated illnesses such as major depressive disorder and post-traumatic stress disorder, increasing interest in identifying immune markers that provide insight into mental health. Recombination events during T-cell receptor rearrangement and T-cell maturation in the thymus produce circular DNA fragments called T-cell receptor excision circles (TRECs) that can be utilized as indicators of thymic function and numbers of newly emigrating T-cells. Given data suggesting that stress affects thymus function, we examined whether blood levels of TRECs might serve as a quantitative peripheral index of cumulative stress exposure and its physiological correlates. We hypothesized that chronic stress exposure would compromise thymus function and produce corresponding decreases in levels of TRECs. In male mice, exposure to chronic social defeat stress (CSDS) produced thymic involution, adrenal hypertrophy, and decreased levels of TRECs in blood. Extending these studies to humans revealed robust inverse correlations between levels of circulating TRECs and childhood emotional and physical abuse. Cell-type specific analyses also revealed associations between TREC levels and blood cell composition, as well as cell-type specific methylation changes in CD4T + and CD8T + cells. Additionally, TREC levels correlated with epigenetic age acceleration, a common biomarker of stress exposure. Our findings demonstrate alignment between findings in mice and humans and suggest that blood-borne TRECs are a translationally-relevant biomarker that correlates with, and provides insight into, the cumulative physiological and immune-related impacts of stress exposure in mammals.

Enhanced endogenous oxytocin signaling in the brain modulates neural responses to social misalignment and promotes conformity in humans: A multi-locus genetic profile approach.

The neuropeptide oxytocin (OT) is known to promote social conformity. However, the specific neurocognitive mechanisms underlying OT-induced conformity remain unclear. We aimed to address this gap by examining how genetic variation in the oxytocin receptor gene (OXTR) is linked with behavioral conformity and its underlying neural systems. Specifically, we utilized the genotype-tissue expression database (GTEx) to create a novel multi-locus genetic profile score (MPS) that reflects the level of OXTR expression in the human brain. A total of 194 participants (Neuroimaging N = 50, Behavioral N = 144) performed a novel conformity task in which they viewed a series of word pairs depicting various moral values and virtues widely recognized in the United States. In each trial, participants indicated the relative importance of these words and subsequently learned about the majority opinion. Participants later rated the same word pairs a second time. Changes in participants' ratings between the first and second sessions were measured and analyzed with respect to social feedback, blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI) signals, and OXTR MPS. We found that participants adjusted their ratings in accordance with the majority opinions. Social misalignment between self and others activated brain areas such as the striatum and the posterior medial frontal cortex (pMFC). However, unlike most findings from previous studies, activation in the pMFC during the inconsistent social feedback negatively, rather than positively, predicted behavioral conformity. Notably, those with higher OXTR MPS had reduced pMFC activation in the face of social misalignment, which led to greater conformity. Our findings suggest that OT may promote conformity by dampening the conflict-related signals in the pMFC. They also show that OXTR MPS may be useful for studying the effect of genes on highly complex human social traits, such as conformity.