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Acute stress potentiates anxiety in humans.

ABSTRACT: BACKGROUND:Stress is an important factor in the development and maintenance of anxiety disorders. Stress also potentiates anxiety-like response in animals, but empirical evidence for a similar effect in humans is still lacking. METHODS:To test whether stress increases anxiety in humans, we examined the ability of a social stressor (speech and a counting task) to potentiate the facilitation of startle in the dark. Measures of subjective distress and of hypothalamic-pituitary-adrenal axis and autonomic nervous system activity (e.g., salivary cortisol, alpha-amylase, blood pressure, and heart rate) were also taken to confirm the effectiveness of the stress manipulation. RESULTS:Startle was significantly facilitated in the dark. This effect was potentiated by prior exposure to the social stressor. The social stressor induced increases in salivary cortisol and alpha amylase as well as increases in blood pressure, heart rate, and subjective distress. CONCLUSION:The findings indicate that stress potentiates anxiety. Animal studies suggest that such an effect might be mediated by glucocorticoid effects on corticotropin-releasing hormone in limbic structures.

SUBMITTER: Grillon C

PROVIDER: S-EPMC2093988 | biostudies-literature | 2007 Nov

REPOSITORIES: biostudies-literature

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Acute stress potentiates anxiety in humans.

Grillon Christian C Duncko Roman R Covington Matthew F MF Kopperman Lori L Kling Mitchel A MA

Biological psychiatry 20070810 10

<h4>Background</h4>Stress is an important factor in the development and maintenance of anxiety disorders. Stress also potentiates anxiety-like response in animals, but empirical evidence for a similar effect in humans is still lacking.<h4>Methods</h4>To test whether stress increases anxiety in humans, we examined the ability of a social stressor (speech and a counting task) to potentiate the facilitation of startle in the dark. Measures of subjective distress and of hypothalamic-pituitary-adrena ...[more]

PMID: 17692829

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Project description:Adolescence is a critical period of heightened stress sensitivity and elevated vulnerability for developing mental illness, suggesting a possible association between stress exposure and the etiology of psychiatric disorders. In adults, aberrant neurobiological responses to acute stress relate to anxiety symptoms, yet less is known about the neural stress response in adolescents and how it relates to biological and psychological variables. Here we characterize the neurobiology of stress response in adolescents using multiple modalities, including neuroimaging, subjective stress ratings, heart rate, and cortisol data. We evaluated stress response in adolescents using the Montreal Imaging Stress Task (MIST), an acute psychosocial stressor commonly administered in adult functional magnetic resonance imaging (fMRI) studies but not previously utilized with this population. FMRI data were acquired from 101 adolescents (44 female; 9-16 years) exhibiting varied trait anxiety severity. The MIST elicited decreased high-frequency heart rate variability and increased heart rate, subjective stress and cortisol. Whole-brain analyses comparing fMRI activity during experimental versus control MIST conditions revealed stress-related activation in regions including the anterior insula, dorsal anterior cingulate cortex, and dorsolateral prefrontal cortex and deactivations in the hippocampus, ventral striatum, and putamen. Region of Interest analyses found that during acute stress (a) hippocampal deactivation corresponded to heightened cortisol release, (b) trait anxiety was associated with increased hippocampal and ventral striatum activation and decreased putamen activity, and (c) males exhibited greater putamen deactivation than females. These results provide novel evidence that the MIST is an effective stressor for adolescents. Associations between the neural acute stress response, other biological factors, and trait anxiety highlight the importance of these neurobiological mechanisms in understanding anxiety disorders.

Project description:Significant evidence suggests that exposure to traumatic and/or acute stress in both mice and humans results in compromised immune function that in turn may affect associated brain processes. Additionally, recent studies in mouse models of immune deficiency have suggested that adaptive immunity may play a role during traumatic stress exposure and that impairments in lymphocyte function may contribute to increased susceptibility to various psychogenic stressors. However, rodent studies on the relationship between maladaptive stress responses and lymphocyte deficiency have been complicated by the fact that genetic manipulations in these models may also result in changes in CNS function due to the expression of targeted genes in tissues other than lymphocytes, including the brain. To address these issues we utilized mice with a deletion of recombination-activating gene 2 (Rag2), which has no confirmed expression in the CNS; thus, its loss should result in the absence of mature lymphocytes without altering CNS function directly. Stress responsiveness of immune deficient Rag2(-/-) mice on a BALB/c background was evaluated in three different paradigms: predator odor exposure (POE), fear conditioning (FC) and learned helplessness (LH). These models are often used to study different aspects of stress responsiveness after the exposure to an acute stressor. In addition, immunoblot analysis was used to assess hippocampal BDNF expression under both stressed and non-stressed conditions. Subsequent to POE, Rag2(-/-) mice exhibited a reduced acoustic startle response compared to BALB/c mice; no significant differences in behavior were observed in either FC or LH. Furthermore, analysis of hippocampal BDNF indicated that Rag2(-/-) mice have elevated levels of the mature form of BDNF compared to BALB/c mice. Results from our studies suggest that the absence of mature lymphocytes is associated with increased resilience to stress exposure in the POE and does not affect behavioral responses in the FC and LH paradigms. These findings indicate that lymphocytes play a specific role in stress responsiveness dependent upon the type, nature and intensity of the stressor.

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Acute stress potentiates anxiety in humans.

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Acute stress potentiates anxiety in humans.

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