Exogenous cortisol exerts effects on the startle reflex independent of emotional modulation

Buchanan, Tony W.; Brechtel, Anette; Sollers, John J.; Lovallo, William R.

doi:10.1016/s0091-3057(00)00450-0

Cited by 81 publications

(62 citation statements)

References 35 publications

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“…(a) Functional magnetic resonance scans following 10 mg intravenous hydrocortisone injection showed rapid uptake (15 min) in the hippocampus and amygdala, resulting in diminished activation of those structures (Lovallo et al, 2010b). (b) Hydrocortisone (20 mg) acutely suppresses the startle reflex (Buchanan et al, 2001a), thereby modulating behavioral responses to sudden, unexpected stimuli during stress episodes. (c) In young adults, hydrocortisone enhanced hippocampal responses to infant cries, an effect that was modulated by previous experience of parental neglect (Bos et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Cortisol Stress Response in Men and Women Modulated Differentially by the Mu-Opioid Receptor Gene Polymorphism OPRM1 A118G

Lovallo

Enoch

Acheson

et al. 2015

Neuropsychopharmacol

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Differences in stress reactivity may affect long-term health outcomes, but there is little information on how these differences arise. The stress axis is regulated by, in part, the endogenous opioid, beta-endorphin, acting on mu-opioid receptors. Persons carrying one or two copies of the G allele of the mu-opioid receptor gene (OPRM1 A118G) may have higher receptor binding for beta-endorphin compared with AA homozygotes that may contribute to individual differences in cortisol reactivity to stress, leading to a relative blunting of cortisol stress reactivity in G allele genotypes. We measured cortisol in 251 young adults (69 GA/GG vs 182 AA genotypes) exposed to mental arithmetic plus public speaking stress relative to a resting control day. Women had smaller cortisol responses than men (F = 10.2, p = 0.002), and women with GA or GG genotypes (N = 39) had an absence of cortisol response relative to AA carriers (N = 110) (F = 18.4, po0.0001). Male genotypes had no such difference in response (F = 0.29). Cortisol response following mu-opioid receptor blockade using naltrexone in 119 of these subjects unmasked a greater tonic opioid inhibition of cortisol secretion in women (N = 64), consistent with their blunted stress reactivity. Compared with men, women may have cortisol stress responses that are more heavily regulated by endogenous opioid mechanisms, and the OPRM1 GA/GG genotypes may affect females differentially relative to males. Diminished cortisol responses to stress may have consequences for health behaviors in women with GA/GG genotypes.

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Section: Discussionmentioning

confidence: 99%

Cortisol Stress Response in Men and Women Modulated Differentially by the Mu-Opioid Receptor Gene Polymorphism OPRM1 A118G

Lovallo

Enoch

Acheson

et al. 2015

Neuropsychopharmacol

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“…Cortisol can alter immune-system responses (26). Its long-term elevation is associated with depression (27) and altered central nervous system responsiveness (28), including sensitization of the limbic system (29), alterations in declarative memory (30), and alterations in frontal lobe function (31).…”

Section: Discussionmentioning

confidence: 99%

Caffeine Stimulation of Cortisol Secretion Across the Waking Hours in Relation to Caffeine Intake Levels

Lovallo

Whitsett

Al’Absi

et al. 2005

Psychosomatic Medicine

119

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Objective-Caffeine increases cortisol secretion in people at rest or undergoing mental stress. It is not known whether tolerance develops in this response with daily intake of caffeine in the diet. We therefore tested the cortisol response to caffeine challenge after controlled levels of caffeine intake.Methods-Men (N = 48) and women (N = 48) completed a double-blind, crossover trial conducted over 4 weeks. On each week, subjects abstained for 5 days from dietary caffeine and instead took capsules totaling 0 mg, 300 mg, and 600 mg/day in 3 divided doses. On day 6, they took capsules with either 0 mg or

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“…There is also some evidence for a direct effect of glucocorticoids on startle responding. In healthy human subjects, exogenous cortisol administration increases startle at low doses and reduces it at high doses (Buchanan et al, 2001). In rats, low doses of corticosterone enhance CRF-induced increases in startle (Lee et al, 1994).…”

Section: Crf Effects On Startlementioning

confidence: 98%

Role of corticotropin releasing factor in anxiety disorders: A translational research perspective

Risbrough

Stein

2006

Hormones and Behavior

211

139

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Anxiety disorders are a group of mental disorders that include generalized anxiety disorder (GAD), panic disorder, phobic disorders (e.g., specific phobias, agoraphobia, social phobia) and posttraumatic stress disorder (PTSD). Anxiety disorders are among the most common of all mental disorders and, when coupled with an awareness of the disability and reduced quality of life they convey, they must be recognized as a serious public health problem. Over 20 years of preclinical studies point to a role for the CRF system in anxiety and stress responses. Clinical studies have supported a model of CRF dysfunction in depression and more recently a potential contribution to specific anxiety disorders (i.e., panic disorder and PTSD). Much work remains in both the clinical and preclinical fields to inform models of CRF function and its contribution to anxiety. First, we will review the current findings of CRF and HPA axis abnormalities in anxiety disorders. Second, we will discuss startle reflex measures as a tool for translational research to determine the role of the CRF system in development and maintenance of clinical anxiety. KeywordsCRH; CRF; Posttraumatic stress disorder; Anxiety; Panic disorder; Startle Overview of CRF neuroendocrine effects and its effects on G-protein-coupled receptorsCorticotropin releasing factor (CRF; also termed "CRH" for corticotropin releasing hormone) was first described in Science by Vale et al. (1981). They reported the discovery of a hypothesized hypothalamic factor, CRF, a 41 amino acid peptide which selectively and potently activated pituitary corticotropin (or adrenal corticotropin releasing hormone, ACTH) secretion. They predicted that this peptide could be "a key signal in mediating and integrating an organism's endocrine, visceral and behavioral response to stress" (Vale et al., 1981(Vale et al., p. 1397). More than 20 years of subsequent animal research and clinical studies have confirmed this hypothesis, supporting a role for CRF, and its more recently discovered ligand family Urocortin 1, 2 and 3, in anxiety and stress responses Reyes et al., 2001;Spina et al., 1996). In this review, we will focus on the current state of knowledge of CRF system dysregulation in clinical anxiety and discuss future avenues of translational research on the role of CRF in startle phenotypes observed in some anxiety disorders. CRF mediation of the neuroendocrine response to stressIn response to stress, CRF is released from the median eminence of the hypothalamus, where it subsequently binds to receptors at the anterior pituitary and increases ACTH release into the * Corresponding author. 8950 Villa La Jolla Drive, Suite B-218, La Jolla, CA 92037, USA. E-mail address: mstein@ucsd.edu (M.B. Stein). bloodstream. ACTH consequently acts at the adrenal cortex to facilitate release of glucocorticoids such as cortisol. This system, known as the hypothalamic-pituitary-adrenal axis (HPA), is an important component of the response to stress and has been shown to be dysregulated in both anxiety and de...

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Exogenous cortisol exerts effects on the startle reflex independent of emotional modulation

Cited by 81 publications

References 35 publications

Cortisol Stress Response in Men and Women Modulated Differentially by the Mu-Opioid Receptor Gene Polymorphism OPRM1 A118G

Cortisol Stress Response in Men and Women Modulated Differentially by the Mu-Opioid Receptor Gene Polymorphism OPRM1 A118G

Caffeine Stimulation of Cortisol Secretion Across the Waking Hours in Relation to Caffeine Intake Levels

Role of corticotropin releasing factor in anxiety disorders: A translational research perspective

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