Endocrinology of the Stress Response

Abstract

The stress response is subserved by the stress system, which is located both in the central nervous system and the periphery. The principal effectors of the stress system include corticotropin-releasing hormone (CRH); arginine vasopressin; the proopiomelanocortin-derived peptides alpha-melanocyte-stimulating hormone and beta-endorphin, the glucocorticoids; and the catecholamines norepinephrine and epinephrine. Appropriate responsiveness of the stress system to stressors is a crucial prerequisite for a sense of well-being, adequate performance of tasks, and positive social interactions. By contrast, inappropriate responsiveness of the stress system may impair growth and development and may account for a number of endocrine, metabolic, autoimmune, and psychiatric disorders. The development and severity of these conditions primarily depend on the genetic vulnerability of the individual, the exposure to adverse environmental factors, and the timing of the stressful events, given that prenatal life, infancy, childhood, and adolescence are critical periods characterized by increased vulnerability to stressors.

Disulfiram enhances subjective effects of dextroamphetamine in humans

“…The endocrine measures of plasma cortisol and prolactin were obtained at baseline and then at one, two, and three hours after dextroamphetamine administration. The measures of cortisol and prolactin were chosen as their release is controlled by the central noradrenergic and dopaminergic pathways, respectively, (Charmandari et al, 2005;Freeman et al, 2000) and both hormones have been shown to be sensitive to amphetamine administration (Grady et al, 1996;Seiden et al, 1993).…”

“…Although the hypothalamic-pituitary-adrenal (HPA) axis including cortisol secretion is enhance by norepinephrine (Charmandari et al, 2005) and prolactin secretion is inhibited by dopamine (Freeman et al, 2000), disulfiram's potential to reduce norepinephrine and increase dopamine did not enhance the dextroamphetamine-induced cortisol or prolactin increases. This lack of effect is probably due to the re-equilibration of these hormonal systems after 4 days of disulfiram induced changes and the relatively more potent acute amphetamine effect on these hormones.…”

“…The endocrine measures of plasma cortisol and prolactin were obtained at baseline and then at one, two, and three hours after dextroamphetamine administration. The measures of cortisol and prolactin were chosen as their release is controlled by the central noradrenergic and dopaminergic pathways, respectively, (Charmandari et al, 2005;Freeman et al, 2000) and both hormones have been shown to be sensitive to amphetamine administration (Grady et al, 1996;Seiden et al, 1993).The physiological measures consisted of systolic and diastolic blood pressure and heart rate, which were measured at baseline then at 30, 60, 90, 120, 150, and 180 minutes after dextroamphetamine administration.The subjective measures were given at baseline, and then at 30, 60, 90, 150, and 180 minutes after the medication treatment and were comprised of the Drug Effects Questionnaire (DEQ), the Addiction Research Center Inventory-Short Form (ARCI), and the Profile of Mood States (POMS). The DEQ assessed the acute subjective effects of dextroamphetamine, and asked subjects to rate "stimulated", "high", "anxious", "sedated", "down", "feeling the drug strength", "feel good drug effects", "feel bad drug effects", "want more drug", and "like the drug" on a 100 mm scale, from 0 ("not at all") to 100 ("extremely").…”

Variation in adrenal and thyroid hormones with life-history stage in juvenile northern elephant seals (Mirounga angustirostris)

“…Activation of the HPA axis is associated with reductions in the release of thyroid stimulating hormone (TSH) and inhibition of conversion of thyroid hormone to biologically active forms (Charmandari et al, 2005). Deiodinase enzymes located within target tissues convert thyroxine (T4) to triiodothryonine (T3), the biologically active form of thyroid hormone or reverse T3 (rT3; Helmreich and Tylee, 2011), which binds to the thyroid receptor without activation.…”

Fearful temperament and stress reactivity among preschool‐aged children

“…This interest reflects an enhanced understanding of the neurobiology of both conditioned (LeDoux & Phelps, 2000) and unconditioned fear (Davis, Walker, & Lee, 1997) and belief that the distributed neural systems underlying acute expressions of fear also support more stable, temperamental variations in fearfulness (Rothbart, 1989). The distributed neural circuits that orchestrate fear behavior have outflows to both arms of the mammalian stress system (Charmandari, Tsigos, & Chrousos, 2005). Specifically, they activate both the autonomic nervous system (ANS) to support fight/flight reactions to threat and the hypothalamic-pituitary-adrenocortical (HPA) system, a counter-regulatory system that has multiple roles in adaptation.…”