Hippocampal gray matter volume in young adulthood varies with adolescent alcohol use.

Adolescent substance use is linked with negative future outcomes (e.g., depression, anxiety, substance use disorder). Given that the brain undergoes significant maturation during adolescence, this developmental period may represent a time of particular vulnerability to substance use. Neuroimaging research has largely focused on heavy or binge patterns of substance use; thus, relatively less is known about the neural impact of a broader range of adolescent substance use. Characterizing the neural impact of a broader range of adolescent substance use may inform prevention and treatment efforts. The present study investigated relationships between adolescent substance use trajectories (i.e., alcohol, tobacco, and cannabis) and gray matter volume in young adulthood. Substance use was assessed in 1,594 participants at ages 11, 13, 16, and 19. Following the last assessment, 320 participants completed a single magnetic resonance imaging session to assess brain gray matter volume. Latent growth curve models were used to estimate growth parameters characterizing alcohol, tobacco, and cannabis use trajectories for each participant. These growth parameters (i.e., intercept, linear slope, and quadratic slope) were then used as predictors of gray matter volume. The gray matter volume of the hippocampus was positively associated with age 14 alcohol use (i.e., intercept) but not other trajectories (i.e., progression or acceleration) or substances (tobacco or cannabis). These results provide new insight into the neural impact of distinct adolescent alcohol, tobacco, and cannabis use trajectories, which may help to refine prevention and treatment efforts. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Hippocampal and amygdala volumes vary with residential proximity to toxicants at Birmingham, Alabama's 35th Avenue Superfund site.

Exposure to environmental toxicants have serious implications for the general health and well-being of children, particularly during pivotal neurodevelopmental stages. The Environmental Protection Agency's (EPA) Superfund program has identified several areas (Superfund sites) across the United States with high levels of environmental toxicants, which affect the health of many residents in nearby communities. Exposure to these environmental toxicants has been linked to changes in the structure and function of the brain. However, limited research has investigated the relationship between the proximity of childhood homes to a Superfund site and the development of subcortical structures like the hippocampus and amygdala. The present study investigated the hippocampal and amygdala volumes of young adults in relation to the proximity of their childhood homes to Birmingham, Alabama's 35th Avenue Superfund site. Forty participants who either lived within or adjacent to the Superfund site (Proximal group; n = 20) or who lived elsewhere in the greater Birmingham metropolitan area (Distal group; n = 20) were included in this study. Both groups were matched on age, sex, race, and years of education. Magnetic resonance imaging (MRI) was used to compare the gray matter volume of the hippocampus and amygdala between groups. Differences in bilateral hippocampal and left amygdala volumes were observed. Specifically, hippocampal and amygdala volumes were greater in the Proximal than Distal group. These findings suggest that the proximity of children's homes to environmental toxicants may impact the development of the hippocampus and amygdala. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Stress-induced Changes in Autonomic Reactivity Vary with Adolescent Violence Exposure and Resting-state Functional Connectivity.

Exposure to violence during childhood can lead to functional changes in brain regions that are important for emotion expression and regulation, which may increase susceptibility to internalizing disorders in adulthood. Specifically, childhood violence exposure can disrupt the functional connectivity among brain regions that include the prefrontal cortex (PFC), hippocampus, and amygdala. Together, these regions are important for modulating autonomic responses to stress. However, it is unclear to what extent changes in brain connectivity relate to autonomic stress reactivity and how the relationship between brain connectivity and autonomic responses to stress varies with childhood violence exposure. Thus, the present study examined whether stress-induced changes in autonomic responses (e.g., heart rate, skin conductance level (SCL)) varied with amygdala-, hippocampus-, and ventromedial prefrontal cortex (vmPFC)-whole brain resting-state functional connectivity (rsFC) as a function of violence exposure. Two hundred and ninety-seven participants completed two resting-state functional magnetic resonance imaging scans prior to (pre-stress) and after (post-stress) a psychosocial stress task. Heart rate and SCL were recorded during each scan. Post-stress heart rate varied negatively with post-stress amygdala-inferior parietal lobule rsFC and positively with post-stress hippocampus-anterior cingulate cortex rsFC among those exposed to high, but not low, levels of violence. Results from the present study suggest that post-stress fronto-limbic and parieto-limbic rsFC modulates heart rate and may underlie differences in the stress response among those exposed to high levels of violence.

Consensus design of a calibration experiment for human fear conditioning.

Fear conditioning is a widely used laboratory model to investigate learning, memory, and psychopathology across species. The quantification of learning in this paradigm is heterogeneous in humans and psychometric properties of different quantification methods can be difficult to establish. To overcome this obstacle, calibration is a standard metrological procedure in which well-defined values of a latent variable are generated in an established experimental paradigm. These intended values then serve as validity criterion to rank methods. Here, we develop a calibration protocol for human fear conditioning. Based on a literature review, series of workshops, and survey of N = 96 experts, we propose a calibration experiment and settings for 25 design variables to calibrate the measurement of fear conditioning. Design variables were chosen to be as theory-free as possible and allow wide applicability in different experimental contexts. Besides establishing a specific calibration procedure, the general calibration process we outline may serve as a blueprint for calibration efforts in other subfields of behavioral neuroscience that need measurement refinement.

Early Life Stress, Coping, and Cardiovascular Reactivity to Acute Social Stress.

OBJECTIVE: Early life stress (ELS) occurring during childhood and adolescence is an established risk factor for later cardiovascular disease and dysregulated reactivity to acute social stress. This study examined whether ELS associations with baseline cardiovascular functioning, cardiovascular stress reactivity and recovery, and emotional stress reactivity vary across levels of emotion-oriented, task-oriented, and avoidant coping styles. METHODS: The sample included 1027 adolescents and young adults (mean age = 19.29 years; 50% female; 64% Black, 34% non-Hispanic White) who reported on their ELS exposure and coping styles. Participants completed a standardized acute social stress test (the Trier Social Stress Test [TSST]), with heart rate (HR) and blood pressure (BP) measured before, during, and after the TSST. Self-reports of negative emotions during the TSST indexed emotional stress reactivity. RESULTS: Multiple regression models adjusting for demographic factors and body mass index showed that ELS was associated with lower HR stress reactivity, avoidant coping was related to lower systolic BP and diastolic BP during stress and lower systolic BP during recovery, and higher emotion-oriented coping and lower task-oriented coping predicted greater emotional stress reactivity. A consistent pattern emerged where emotion-oriented coping amplified the associations between ELS and maladaptive stress responses (blunted cardiovascular stress reactivity and recovery; enhanced emotional stress reactivity), whereas lower levels of emotion-oriented coping were associated with resilient profiles among those who experienced ELS (lower resting HR, lower emotional stress reactivity, average HR and BP stress reactivity and recovery). However, low levels of emotion-oriented coping also conferred a risk of higher BP during recovery for those with high levels of ELS. CONCLUSIONS: These results suggest that low to moderate levels of emotion-oriented coping promote optimal cardiovascular and emotional reactivity to acute stress among individuals exposed to ELS.

Insomnia and post-traumatic stress disorder: A meta-analysis on interrelated association (n = 57,618) and prevalence (n = 573,665).

Posttraumatic stress disorder (PTSD) is a common mental disorder, which is strongly associated with insomnia, yet their epidemiological overlap is poorly understood. To determine the convergent quantitative magnitude of their relationship, PubMed, EMBASE, Scopus, Web of Science, PubPsych, and PsycINFO were searched to identify studies that either reported the correlation or frequency of insomnia symptoms in PTSD and posttraumatic stress symptoms (PTSS), or both. Out of 3714 records, 75 studies met selection criteria and aggregate effect size (ES) estimates were generated for the correlations (K=44, comprising 57,618 subjects) and frequencies (K=33, comprising 573,665 subjects with PTSD/PTSS) of insomnia symptoms in PTSD/PTSS. A medium-size significant correlation was found [ES: 0.52 (CI: 0.47-0.57)] with moderating effects of the COVID-19 pandemic and military service as causes of trauma. The prevalence of insomnia in PTSD/PTSS was 63% [CI: 45%-78%] and was moderated by the cause of trauma as well as the PTSD/PTSS assessment scale. The findings from this meta-analysis highlight the importance of screening and managing insomnia in PTSD patients.

Sex-related differences in violence exposure, neural reactivity to threat, and mental health.

The prefrontal cortex (PFC), hippocampus, and amygdala play an important role in emotional health. However, adverse life events (e.g., violence exposure) affect the function of these brain regions, which may lead to disorders such as depression and anxiety. Depression and anxiety disproportionately affect women compared to men, and this disparity may reflect sex differences in the neural processes that underlie emotion expression and regulation. The present study investigated sex differences in the relationship between violence exposure and the neural processes that underlie emotion regulation. In the present study, 200 participants completed a Pavlovian fear conditioning procedure in which cued and non-cued threats (i.e., unconditioned stimuli) were presented during functional magnetic resonance imaging. Violence exposure was previously assessed at four separate time points when participants were 11-19 years of age. Significant threat type (cued versus non-cued) × sex and sex × violence exposure interactions were observed. Specifically, women and men differed in amygdala and parahippocampal gyrus reactivity to cued versus non-cued threat. Further, dorsolateral PFC (dlPFC) and inferior parietal lobule (IPL) reactivity to threat varied positively with violence exposure among women, but not men. Similarly, threat-elicited skin conductance responses varied positively with violence exposure among women. Finally, women reported greater depression and anxiety symptoms than men. These findings suggest that sex differences in threat-related brain and psychophysiological activity may have implications for mental health.

Development of Dynamic Measures to Assess Balance Confidence and State Anxiety While Walking at Increasing Speeds in Young and Older Adults.

The purpose of this study was to determine the test-retest reliability and construct validity of tools to assess how balance confidence (BC) and state anxiety (SA) change with progressively increasing walking speeds. Sixteen young adults and 15 older adults attended two sessions. Individuals began walking on a treadmill at 0.4 m/s Participants chose to continue increasing the treadmill speed (up to 2.0 m/s) or to discontinue the protocol while rating their BC and SA after completing each speed. BC at participants' fastest speed attempted demonstrated high and moderate test-retest reliability among young (intraclass correlation coefficient [ICC] = .908) and older adults (ICC = .704). SA for young adults and older adults was good (ICC = .833) and fair (ICC = .490), respectively. Our measures also correlated with measures of dynamic stability while walking for young (r = -.67, p = .008) and older adults (r = .54, p = .046). Our dynamic measures of BC and SA are valid and reliable in young and older adults.

Stress-Induced Changes in Effective Connectivity During Regulation of the Emotional Response to Threat.

Background: Stress-related disruption of emotion regulation appears to involve the prefrontal cortex (PFC) and amygdala. However, the interactions between brain regions that mediate stress-induced changes in emotion regulation remain unclear. The present study builds upon prior work that assessed stress-induced changes in the neurobehavioral response to threat by investigating effective connectivity between these brain regions. Methods: Participants completed the Montreal Imaging Stress Task followed by a Pavlovian fear conditioning procedure during functional magnetic resonance imaging. Stress ratings and psychophysiological responses were used to assess stress reactivity. Effective connectivity during fear conditioning was identified using multivariate autoregressive modeling. Effective connectivity values were calculated during threat presentations that were either predictable (preceded by a warning cue) or unpredictable (no warning cue). Results: A neural hub within the dorsomedial PFC (dmPFC) showed greater effective connectivity to other PFC regions, inferior parietal lobule, insula, and amygdala during predictable than unpredictable threat. The dmPFC also showed greater connectivity to different dorsolateral PFC and amygdala regions during unpredictable than predictable threat. Stress ratings varied with connectivity differences from the dmPFC to the amygdala. Connectivity from dmPFC to amygdala was greater in general during unpredictable than predictable threat, however, this connectivity increased during predictable compared with unpredictable threat as stress reactivity increased. Conclusions: Our findings suggest that acute stress disrupts connectivity underlying top-down emotion regulation of the threat response. Furthermore, increased connectivity between the dmPFC and amygdala may play a critical role in stress-induced changes in the emotional response to threat. Impact statement The present study builds upon prior work that assessed stress-induced changes in the human neurobehavioral response to threat by demonstrating that increased top-down connectivity from the dorsomedial prefrontal cortex to the amygdala varies with individual differences in stress reactivity. These findings provide novel evidence in humans of stress-induced disruption of a specific top-down corticolimbic circuit during active emotion regulation processes, which may play a causal role in the long-term effects of chronic or excessive stress exposure.

White Matter Microstructure in the Young Adult Brain Varies with Neighborhood Disadvantage in Adolescence.

Neighborhood disadvantage and community violence are common in poor, urban communities and are risk factors for emotional dysfunction. Emotional processes are supported by neural circuitry that includes the prefrontal cortex (PFC), hippocampus, amygdala, and hypothalamus. These brain regions are connected by white matter pathways that include the cingulum bundle, uncinate fasciculus, stria terminalis, and fornix. Emotional function varies with the microstructure of these white matter pathways. However, it is not clear whether the microstructure of these pathways varies with risk factors for emotional dysfunction (e.g., neighborhood disadvantage and violence exposure). Therefore, determining the relationships between neighborhood disadvantage, violence exposure, and white matter microstructure may offer insight into the neural mechanisms by which adverse life experiences alter developing neural systems. The current study investigated the association that exposure to neighborhood disadvantage and violence have with the quantitative anisotropy (QA), a measure of the amount of directional water diffusion, of the cingulum bundle, uncinate fasciculus, stria terminalis, and fornix. Neighborhood disadvantage (Mage = 11.20) and violence exposure (MW1age = 11.20; MW2age = 13.05; MW3age = 16.20; MW4age = 19.25) were assessed during adolescence and participants returned for magnetic resonance imaging as young adults (N = 303; Mage = 20.25, SD = 1.55), during which diffusion weighted brain images were collected. The QA of the cingulum bundle, uncinate fasciculus, and stria terminalis/fornix varied negatively with neighborhood disadvantage such that the QA of these white matter tracts decreased as neighborhood disadvantage increased. Violence exposure was not related to QA in any tract (i.e., cingulum bundle, uncinate fasciculus, and stria terminalis/fornix) after correction for multiple comparisons. These results suggest that an adolescent's neighborhood may play an important role in the microstructure (i.e., QA) of white matter pathways that connect brain regions that support emotional function.

Hippocampal volume varies with acute posttraumatic stress symptoms following medical trauma.

The hippocampus and amygdala play an important role in the pathophysiology of posttraumatic stress disorder (PTSD). In fact, chronic PTSD has been consistently linked to reductions in hippocampal and amygdala volume. However, the acute impact posttraumatic stress has on the volume of these brain regions has received limited attention. Determining the acute impact posttraumatic stress has on brain volume may improve our understanding of the development of PTSD. Therefore, the present study recruited participants acutely (i.e., ∼1-month posttrauma) following trauma exposure and examined the relationship between brain volume (assessed at ∼1-month posttrauma) and posttraumatic stress symptoms (assessed at ∼1 and >3-months posttrauma) to determine whether brain volume was associated with acute posttraumatic stress symptom expression. Twenty-one trauma-exposed (TE) patients and 19 nontrauma-exposed (NTE) controls were recruited for the present study. Brain volume was assessed by structural magnetic resonance imaging completed during the ∼1-month assessment. Left hippocampal volumes were smaller in TE than NTE participants. Among TE participants, bilateral hippocampal volumes decreased as the number of days posttrauma increased. Further, bilateral hippocampal volumes varied negatively with the severity of posttraumatic stress symptoms at ∼1-month posttrauma. The present findings suggest that there is a progressive decrease in hippocampal volume acutely (e.g., within approximately 1 month) following trauma exposure, and demonstrates that acutely assessed hippocampal volumes vary with posttraumatic stress symptom expression. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Stress-elicited neural activity in young adults varies with childhood sexual abuse.

OBJECTIVE: Childhood physical and sexual abuse are stressful experiences that may alter the emotional response to future stressors. Stress-related emotional function is supported by brain regions that include the prefrontal cortex (PFC), hippocampus, and amygdala. The present study investigated whether childhood physical and sexual abuse are associated with stress-elicited brain activity in young adulthood. METHODS: Participants (N = 300; Mage = 20.0; 151 female) completed a psychosocial stress task during functional magnetic resonance imaging (fMRI). Measures of physical and sexual abuse were included in a linear mixed effects model to estimate the unique relationship each type of childhood abuse had with stress-elicited brain activity. RESULTS: Stress-elicited dorsolateral PFC, ventromedial PFC, and hippocampal activity decreased as the frequency of childhood sexual abuse increased. There were no regions in which stress-elicited activation varied with physical abuse. CONCLUSIONS: The present findings suggest there is a unique relationship between childhood sexual abuse and the stress-elicited PFC and hippocampal activity of young adults that is not observed following childhood physical abuse. SIGNIFICANCE: These findings may have important implications for understanding the mechanisms by which childhood sexual abuse impacts the development of future psychopathology.

Violence exposure, affective style, and stress-induced changes in resting state functional connectivity.

Chronic childhood stress is linked to greater susceptibility to internalizing disorders in adulthood. Specifically, chronic stress leads to changes in brain connectivity patterns, and, in turn, affects psychological functioning. Violence exposure, a chronic stressor, increases stress reactivity and disrupts emotion regulation processes. However, it is unclear to what extent violence exposure affects the neural circuitry underlying emotion regulation. Individual differences in affective style also moderate the impact of stress on psychological function and can thus alter the relationship between violence exposure and brain function. Resting-state functional connectivity (rsFC) is an index of intrinsic brain activity. Stress-induced changes in rsFC between the amygdala, hippocampus, and prefrontal cortex (PFC) are associated with emotion dysregulation and may elucidate how affective style modulates the relationship between violence exposure and brain connectivity. Therefore, the present study examined the impact of violence exposure and affective style on stress-induced changes in rsFC. Participants (n = 233) completed two 6-minute resting-state functional magnetic resonance imaging scans, one before (pre-stress) and one after (post-stress) a psychosocial stress task. The bilateral amygdala, hippocampus, and ventromedial prefrontal cortex (vmPFC) were used as seed regions for rsFC analyses. Significant stress-induced changes in the prefrontal, fronto-limbic, and parieto-limbic rsFC were observed. Further, pre-stress to post-stress differences in rsFC varied with violence exposure and affective style. These findings suggest that prefrontal, fronto-limbic, and parieto-limbic connectivity is associated with the emotional response to stress and provide new insight into the neural mechanisms through which affective style moderates the impact violence exposure has on the brain.

PTSD-related neuroimaging abnormalities in brain function, structure, and biochemistry.

Although approximately 90% of the U.S. population will experience a traumatic event within their lifetime, only a fraction of those traumatized individuals will develop posttraumatic stress disorder (PTSD). In fact, approximately 7 out of 100 people in the U.S. will be afflicted by this debilitating condition, which suggests there is substantial inter-individual variability in susceptibility to PTSD. This uncertainty regarding who is susceptible to PTSD necessitates a thorough understanding of the neurobiological processes that underlie PTSD development in order to build effective predictive models for the disorder. In turn, these predictive models may lead to the development of improved diagnostic markers, early intervention techniques, and targeted treatment approaches for PTSD. Prior research has characterized a fear learning and memory network, centered on the prefrontal cortex, hippocampus, and amygdala, that plays a key role in the pathology of PTSD. Importantly, changes in the function, structure, and biochemistry of this network appear to underlie the cognitive-affective dysfunction observed in PTSD. The current review discusses prior research that has demonstrated alterations in brain function, structure, and biochemistry associated with PTSD. Further, the potential for future research to address current gaps in our understanding of the neural processes that underlie the development of PTSD is discussed. Specifically, this review emphasizes the need for multimodal neuroimaging research and investigations into the acute effects of posttraumatic stress. The present review provides a framework to move the field towards a comprehensive neurobiological model of PTSD.

Reproducibility of whole-brain temperature mapping and metabolite quantification using proton magnetic resonance spectroscopy.

Assessing brain temperature can provide important information about disease processes (e.g., stroke, trauma) and therapeutic effects (e.g., cerebral hypothermia treatment). Whole-brain magnetic resonance spectroscopic imaging (WB-MRSI) is increasingly used to quantify brain metabolites across the entire brain. However, its feasibility and reliability for estimating brain temperature needs further validation. Therefore, the present study evaluates the reproducibility of WB-MRSI for temperature mapping as well as metabolite quantification across the whole brain in healthy volunteers. Ten healthy adults were scanned on three occasions 1 week apart. Brain temperature, along with four commonly assessed brain metabolites-total N-acetyl-aspartate (tNAA), total creatine (tCr), total choline (tCho) and myo-inositol (mI)-were measured from WB-MRSI data. Reproducibility was evaluated using the coefficient of variation (CV). The measured mean (range) of the intra-subject CVs was 0.9% (0.6%-1.6%) for brain temperature mapping, and 4.7% (2.5%-15.7%), 6.4% (2.4%-18.9%) and 14.2% (4.4%-52.6%) for tNAA, tCho and mI, respectively, with reference to tCr. Consistently larger variability was found when using H2 O as the reference for metabolite quantifications: 7.8% (3.3%-17.8%), 7.8% (3.1%-18.0%), 9.8% (3.7%-31.0%) and 17.0% (5.9%-54.0%) for tNAA, tCr, tCho and mI, respectively. Further, the larger the brain region (indicated by a greater number of voxels within that region), the better the reproducibility for both temperature and metabolite estimates. Our results demonstrate good reproducibility of whole-brain temperature and metabolite measurements using the WB-MRSI technique.

White matter microstructure varies with post-traumatic stress severity following medical trauma.

The prefrontal cortex, amygdala, hippocampus, and hypothalamus are important components of the neural network that mediates the healthy learning, expression, and regulation of emotion. These brain regions are connected by white matter pathways that include the cingulum bundle, uncinate fasciculus, and fornix/stria terminalis. Individuals with trauma and stress-related disorders show dysfunction of the cognitive-affective processes supported by the brain regions these white matter tracts connect. Therefore, variability in the microstructure of these white matter pathways may play an important role in the cognitive-affective dysfunction related to post-traumatic stress disorder. Thus, the current study used diffusion weighted imaging to assess the white matter microstructure of the cingulum bundle, uncinate fasciculus, and fornix/stria terminalis acutely (< 1 month) following trauma. Further, we assessed both acute (i.e., < 1 month) and subacute (i.e., 3 months post-trauma) post-traumatic stress symptom severity. White matter microstructure (assessed < 1 month post-trauma) of the uncinate fasciculus and fornix/stria terminalis varied with acute post-traumatic stress severity (assessed < 1 month post-trauma). Further, white matter microstructure (assessed < 1 month post-trauma) of the cingulum bundle and fornix/stria terminalis varied with subacute post-traumatic stress severity (assessed 3 months post-trauma). The current results suggest white matter architecture of the prefrontal cortex - amygdala network plays an important role in the development of trauma and stress-related disorders.

Negative life experiences contribute to racial differences in the neural response to threat.

Threat-related emotional function is supported by a neural circuit that includes the prefrontal cortex (PFC), hippocampus, and amygdala. The function of this neural circuit is altered by negative life experiences, which can potentially affect threat-related emotional processes. Notably, Black-American individuals disproportionately endure negative life experiences compared to White-American individuals. However, the relationships among negative life experiences, race, and the neural substrates that support threat-related emotional function remains unclear. Therefore, the current study investigated whether the brain function that supports threat-related emotional processes varies with racial differences in negative life experiences. In the present study, adolescent violence exposure, family income, and neighborhood disadvantage were measured prospectively (i.e., at 11-19 years of age) for Black-American and White-American volunteers. Participants then, as young adults (i.e., 18-23 years of age), completed a Pavlovian fear conditioning task during functional magnetic resonance imaging (fMRI). Cued and non-cued threats were presented during the conditioning task and behavioral (threat expectancy) and psychophysiological responses (skin conductance response; SCR) were recorded simultaneously with fMRI. Racial differences were observed in neural (fMRI activity), behavioral (threat expectancy), and psychophysiological (SCR) responses to threat. These threat-elicited responses also varied with negative life experiences (violence exposure, family income, and neighborhood disadvantage). Notably, racial differences in brain activity to threat were smaller after accounting for negative life experiences. The present findings suggest that racial differences in the neural and behavioral response to threat are due, in part, to exposure to negative life experiences and may provide new insight into the mechanisms underlying racial disparities in mental health.

Amygdala and prefrontal cortex activity varies with individual differences in the emotional response to psychosocial stress.

Stress elicits a variety of psychophysiological responses that show large interindividual variability. Determining the neural mechanisms that mediate individual differences in the emotional response to stress would provide new insight that would have important implications for understanding stress-related disorders. Therefore, the present study examined individual differences in the relationship between brain activity and the emotional response to stress. In the largest stress study to date, 239 participants completed the Montreal Imaging Stress Task (MIST) while heart rate, skin conductance response (SCR), cortisol, self-reported stress, and blood oxygen level dependent (BOLD) functional MRI (fMRI) signal responses were measured. The relationship between differential responses (heart rate, SCR, cortisol, and self-reported stress) and differential BOLD fMRI data was analyzed. Dorsolateral prefrontal cortex (PFC), dorsomedial PFC, ventromedial PFC, and amygdala activity varied with the behavioral response (i.e., SCR and self-reported stress). These results suggest the PFC and amygdala support processes that are important for the expression and regulation of the emotional response to stress, and that stress-related PFC and amygdala activity underlie interindividual variability in peripheral physiologic measures of the stress response. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Emotion Socialization and Internalizing Problems in Late Adolescence and Emerging Adulthood: Coping Styles as Mediators.

This study examined coping strategies as mediators of the relationship between parental emotion socialization and internalizing problems in late adolescence and emerging adulthood, and whether these relationships varied by gender or ethnicity. Participants were 1,087 individuals (Mage = 19.35 years; 50% male; 61% African American, 36% European American). Results from structural equation modeling indicated that parental supportive responses to sadness and fear were associated with less emotional distress, and this relationship was partly mediated by greater use of task-oriented coping and lower use of emotion-oriented coping. Parental unsupportive responses were related to greater emotional distress, and this relationship was fully mediated by greater use of emotion-oriented coping. Gender and ethnic differences emerged in the links between parental responses and several coping strategies. The findings suggest that parental emotion socialization may contribute to emotional functioning by fostering specific coping strategies, with some differences across gender and ethnicity.