Reactivity In Healthy Adults Research Articles

Amygdala Reactivity in Healthy Adults Is Correlated with Prefrontal Cortical Thickness

Recent evidence suggests that putting feelings into words activates the prefrontal cortex (PFC) and suppresses the response of the amygdala, potentially helping to alleviate emotional distress. To further elucidate the relationship between brain structure and function in these regions, structural and functional magnetic resonance imaging (MRI) data were collected from a sample of 20 healthy human subjects. Structural MRI data were processed using cortical pattern-matching algorithms to produce spatially normalized maps of cortical thickness. During functional scanning, subjects cognitively assessed an emotional target face by choosing one of two linguistic labels (label emotion condition) or matched geometric forms (control condition). Manually prescribed regions of interest for the left amygdala were used to extract percentage signal change in this region occurring during the contrast of label emotion versus match forms. A correlation analysis between left amygdala activation and cortical thickness was then performed along each point of the cortical surface, resulting in a color-coded r value at each cortical point. Correlation analyses revealed that gray matter thickness in left ventromedial PFC was inversely correlated with task-related activation in the amygdala. These data add support to a general role of the ventromedial PFC in regulating activity of the amygdala.

Serotonin transporter and BDNF genetic variants interact to predict cognitive reactivity in healthy adults

Background Cognitive theory and empirical evidence both suggest that cognitive reactivity (the tendency to think more negatively when in a sad mood) is an important marker of depression vulnerability. Research has not yet determined whether genetic factors contribute to the expression of cognitive reactivity. Methods The present study examined associations between the 5-HTTLPR polymorphism of the SLC6A4 gene, the Val66Met polymorphism of the brain-derived neurotrophic factor (BDNF) gene, and cognitive reactivity in a never depressed, unmedicated, young adult sample ( N = 151). Results The interaction between 5-HTTLPR and Val66Met polymorphisms significantly predicted change in dysfunctional thinking from before to after a standardized sad mood provocation. Cognitive reactivity increased among S/L G 5-HTTLPR homozygotes if they were also homozygous for the Val Val66Met allele. In contrast, presence of a Met Val66Met allele was associated with attenuated cognitive reactivity among S/L G 5-HTTLPR homozygotes. Limitations The sample size of the current study is relatively small for modern genetic association studies. However, results are consistent with previous research demonstrating biological epistasis between SLC6A4 and BDNF for predicting connectivity among neural structures involved in emotion regulation. Conclusions The BDNF Met allele may protect S/L G 5-HTTLPR homozygotes from increased dysfunctional thinking following a sad mood provocation. Study results are the first to demonstrate an epistatic genetic relationship predicting cognitive reactivity and suggest the need for more complex and integrative models of depression vulnerability.

Relationships between psychological distress, coping styles, and HPA axis reactivity in healthy adults

Psychological distress and coping styles have been suggested to relate to altered function in the hypothalamic-pituitary-adrenal (HPA) axis, although there remains much to be understood about their relationships. High and low cortisol levels (or reactivity) both represent HPA axis dysfunction, with accumulated evidence suggesting that they are linked to different types of psychopathology. The dexamethasone (DEX)/corticotropin-releasing hormone (CRH) test has been extensively used to identify HPA axis abnormalities in various psychiatric conditions including mood disorders; however, the possible associations of psychological distress and coping styles with HPA axis function have not been well documented using this test. Here, we examined the relationships of HPA axis reactivity as measured by the DEX/CRH test with subjectively perceived psychological distress and coping styles, both of which were assessed with self-report questionnaires, in 121 healthy volunteers. Subjects were divided into three groups by the cortisol suppression pattern, namely the incomplete-suppressors (DST-Cortisol ≥ 5 μg/dL or DEX/CRH-Cortisol ≥ 5 μg/dL), moderate-suppressors (DST-Cortisol < 5 μg/dL and 1 μg/dL ≤ DEX/CRH -Cortisol < 5 μg/dL), and enhanced-suppressors (DST-Cortisol < 5 μg/dL and DEX/CRH-Cortisol < 1 μg/dL). The enhanced-suppressors showed significantly higher scores in obsessive-compulsive, interpersonal sensitivity and anxiety symptoms and significantly more frequent use of avoidant coping strategy, compared to the other two groups. These results point to the important role of enhanced suppression of cortisol, or blunted cortisol reactivity, in non-clinical psychopathology such as avoidant coping strategy and greater psychological distress.

Frontal electrocortical and cardiovascular reactivity during happiness and anger

The present study investigated electrocortical and cardiovascular reactivity during positive and negative emotion, and examined the relation of asymmetric frontal lobe activation to cardiovascular responses. Participants were 30 healthy, right-handed university students (mean age, 23.9; 60% female; 76% Caucasian). Electroencephalographic (EEG), blood pressure (BP), and heart rate (HR) responses were assessed while subjects engaged in laboratory tasks (personally-relevant recall tasks and film clips) designed to elicit happiness or anger. Happiness-inducing tasks evoked more prominent left than right frontal EEG activation, and greater left frontal EEG activation than anger-inducing tasks. However, anger-inducing tasks were, on average, associated with comparable left and right frontal EEG activation. Irrespective of emotional valence, cardiovascular activation was more pronounced during personally-relevant recall tasks than during the viewing of film clips. During anger recall, both greater left frontal EEG response ( r=−0.46, P<0.02) and greater right frontal EEG response ( r=−0.45, P<0.02) were correlated significantly with increased HR reactivity during the task. In addition, a right lateralized frontal EEG response during anger-inducing tasks was associated with greater concomitant systolic BP ( P<0.03) and diastolic BP ( P<0.008) reactivity. Exploratory analyses also indicated that men who displayed a left lateralized frontal EEG response during happiness-inducing tasks showed the greatest concomitant systolic BP and HR reactivity ( P's<0.03). These findings suggest that asymmetric frontal EEG responses to emotional arousal may elicit different patterns of cardiovascular reactivity in healthy adults.

Research connections

Two studies are reviewed, one regarding the effects of music therapy on psychophysiologic stress in coronary care unit patients and one regarding the effects of age and gender on cardiovascular autonomic reactivity in healthy adults. Music therapy is determined to be safe for coronary care unit patients and effective in modulating the psychophysiologic manifestations of stress. The second study suggests that age--gender interactions may influence autonomic cardiovascular responsiveness. It is suggested that older adults be taught methods to reduce straining, so that rapid transient changes in blood pressure are avoided.

Beta-adrenergic responses and airway reactivity in healthy adults

Healthy adults aged 18–90 years were tested for lymphocyte and granulocyte cyclic AMP responses to isoproterenol and prostaglandin E 1 (PGE 1), beta-adrenergic receptor density and antagonist binding properties, and for airway reactivity to methacholine. Our hypothesis was that reduced beta-adrenergic responses occur with aging and are associated with increased airway reactivity. This hypothesis was not supported by the data. Lymphocyte stimulation ratios (cyclic AMP level with stimulation/baseline cyclic AMP level) at higher concentrations of isoproterenol and PGE 1 increased significantly with age. There were no significant age trends for any of the other variables. None of the beta-adrenergic responses or receptor properties correlated with airway reactivity to methacholine. Beta-adrenergic responses in lymphocyte and granulocytes from the same subject were weakly correlated at high concentrations. Prior studies which suggest that reduced beta-adrenergic responses and increased airway reactivity are concomitants of normal aging may differ from the present study in subject selection. In healthy older subjects, there appears to be no reduction in leukocyte beta-adrenergic responses or receptor properties and no change in airway reactivity.