Glucocorticoid Physiology, Pharmacology and Stress

Munck, Allan; Guyre, Paul M.

doi:10.1007/978-1-4684-5101-6_6

Cited by 140 publications

(94 citation statements)

References 13 publications

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Section: Abstract: Alcohol; Acth; Corticosterone; C-fos; Ngfi-b; Pvnmentioning

confidence: 99%

“…Glucocorticoids (GC), for example, promote the availability of energy substrates and modulate vascular tone (see Munck and Guyre, 1986). After antigenic challenges and once appropriate defense mechanisms have become activated, GC serve to restrain the activity of the immune system and thus prevent it from overshooting (Munck and Guyre, 1986). Corticotropin-releasing factor (CRF), on the other hand, regulates behavior (Koob, 1990) and sympathetic activity (Brown and Fisher, 1990), as well as appetite and gastrointestinal functions (Taché et al, 1993), immune responses, and reproductive and cardiovascular parameters (see Munck et al, 1984;McEwen, 1992;Rivest and Rivier, 1995).…”

Section: Abstract: Alcohol; Acth; Corticosterone; C-fos; Ngfi-b; Pvnmentioning

confidence: 99%

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An Initial, Three-Day-Long Treatment with Alcohol Induces a Long-Lasting Phenomenon of Selective Tolerance in the Activity of the Rat Hypothalamic–Pituitary–Adrenal Axis

Lee

Rivier

1997

J. Neurosci.

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We determined whether an initial alcohol challenge induced long-lasting changes in the activity of the hypothalamic-pituitary-adrenal (HPA) axis. Adult male rats received intragastric injections of the vehicle or a moderately intoxicating dose of alcohol (3.0 gm/kg) daily for 3 d. When animals were acutely challenged with alcohol 3-12 d later, their ACTH and corticosterone responses were significantly blunted, compared with that of vehicle-pretreated rats. In contrast, exposure to mild electric foot shocks induced a pattern of ACTH secretion that was comparable in animals administered alcohol or the vehicle previously, indicating a lack of cross-tolerance. No significant differences were observed in pituitary responsiveness to corticotropin-releasing factor or vasopressin in rats pretreated with the vehicle or alcohol. The influence of the initial drug treatment was not mimicked by exposure to foot shocks, nor was it prevented by administering a potent corticotropinreleasing factor antagonist to block the elevations in plasma ACTH and corticosterone induced by this initial treatment. Finally, we found that rats injected initially with the vehicle and challenged subsequently with alcohol exhibited the expected increased neuronal activation (measured by the upregulation of steady-state mRNA and protein levels of immediate early genes) in the paraventricular nucleus of their hypothalamus. In contrast, this response was markedly decreased in animals exposed previously to the drug.To our knowledge, this is the first report that exposure to a stress (i.e., alcohol), although not immediately altering the response of the HPA axis to this particular signal, induces a selective tolerance that is both slow to develop and longlasting. The primary mechanism mediating the ability of an initial drug treatment to decrease subsequent responses of the HPA axis to a second drug challenge seems to be the inability of hypothalamic neurons to respond adequately to this second challenge.

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Section: Abstract: Alcohol; Acth; Corticosterone; C-fos; Ngfi-b; Pvnmentioning

confidence: 99%

Section: Abstract: Alcohol; Acth; Corticosterone; C-fos; Ngfi-b; Pvnmentioning

confidence: 99%

An Initial, Three-Day-Long Treatment with Alcohol Induces a Long-Lasting Phenomenon of Selective Tolerance in the Activity of the Rat Hypothalamic–Pituitary–Adrenal Axis

Lee

Rivier

1997

J. Neurosci.

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“…ACUTE PSYCHOLOGICAL STRESS is known to activate the hypothalamic-pituitary-adrenal (HPA) axis, resulting in transiently increased release of inflammatory cytokines (28) and glucocorticoids (45). In contrast, multiple exposures to stress lead to adaptive responses in target tissues such as liver, skeletal muscle, and immune cells.…”

mentioning

confidence: 99%

Illuminating the interrelated immune and endocrine adaptations after multiple exposures to short immobilization stress by in vivo blocking of IL-6

Smith¹,

Wilson²,

Louw³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Intermittent psychological stress was induced in adult rats by 2 h/day of immobilization stress for 4 days, with or without blocking the function of IL-6 by using an anti-IL-6 antibody. Basal concentrations of serum corticosterone, IL-1β, IL-6, and TNF-α were assessed 24 h after the last intervention, as were levels of glucocorticoid receptors (GR) and activities of glucocorticoid-inducible enzymes (tyrosine aminotransferase and glutamine synthetase) in muscle and liver. Whole blood cultures were used to assess both spontaneous and LPS-induced reactivity of peripheral blood mononuclear cells. Stress increased corticosterone concentration in a manner partially modulated by IL-6. Serum IL-1β concentration was downregulated during stress when IL-6 was blocked ( P < 0.01). LPS-induced IL-6 secretion by peripheral blood mononuclear cells in vitro correlated positively with serum IL-1β concentration in antibody-treated groups, independently of stress ( R = 0.70 in nonstressed and R = 0.78 in stressed rats; both P < 0.05), whereas serum corticosterone concentration correlated positively with LPS-induced secretion of IL-6 only in control rats ( R = 0.66; P < 0.05). Reductions in liver GR levels indicated independent effects of stress (34.5%) and anti-IL-6 antibody (16.7%) and additive effects for both (62.5%). Similar results are reported for vastus muscle. Conversely, stress increased tyrosine aminotransferase and glutamine synthetase activities in muscle and liver with a significant ( P < 0.05) effect of anti-IL-6 antibody only seen in stressed livers. In conclusion, IL-6 plays a role in maintaining circulating IL-1β concentration after multiple exposures to stress, thus promoting a continued elevation of corticosterone release; in peripheral tissues, IL-6 antagonizes the effects of glucocorticoids, especially at the level of GR concentration.

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“…4). In this acute inflammatory situation, the anti-inflammatory properties of cortisol (45,46) and DHEA (19-23, 47, 48) are probably important to dampen inflammation in the periphery (49). Thus, presence of these hormones is crucial for termination of the acute inflammatory state.…”

Section: Discussionmentioning

confidence: 99%

Dehydroepiandrosterone in relation to other adrenal hormones during an acute inflammatory stressful disease state compared with chronic inflammatory disease: role of interleukin-6 and tumour necrosis factor

Straub

Lehle

Herfarth

et al. 2002

European Journal of Endocrinology

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Objective: Serum levels of dehydroepiandrosterone (DHEA) and DHEA sulphate (DHEAS) are low in chronic inflammatory diseases, although the reasons are unexplained. Furthermore, the behaviour of serum levels of these hormones during an acute inflammatory stressful disease state is not well known. Subjects and methods: In this study in patients with an acute inflammatory stressful disease state (13 patients undergoing cardiothoracic surgery) and patients with chronic inflammation (61 patients with inflammatory bowel diseases (IBD)) vs 120 controls, we aimed to investigate adrenal hormone shifts looking at serum levels of DHEA in relation to other adrenal hormones. Furthermore, we tested the predictive role of serum tumour necrosis factor (TNF) and interleukin-6 (IL-6) for a change of serum levels of DHEA in relation to other adrenal hormones. Results: The molar ratio of serum levels of DHEA/androstenedione (ASD) was increased in patients with an acute inflammatory stressful disease state and was decreased in patients with chronic inflammation. The molar ratio of serum levels of DHEAS/DHEA was reduced during an acute inflammatory stressful disease state and was increased in patients with chronic inflammation. A multiple linear regression analysis revealed that elevated serum levels of TNF were associated with a high ratio of serum levels of DHEA/ASD in all groups (for IL-6 in patients with an acute inflammatory stressful disease state only), and, similarly, elevated serum levels of TNF were associated with a high ratio of serum levels of DHEAS/DHEA only in IBD (for IL-6 only in healthy subjects). Conclusions: This study indicates that changes of serum levels of DHEA in relation to serum levels of other adrenal hormones are completely different in patients with an acute inflammatory stressful disease state compared with patients with chronic inflammation. The decrease of serum levels of DHEAS and DHEA is typical for chronic inflammation and TNF and IL-6 play a predictive role for these changes.

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Glucocorticoid Physiology, Pharmacology and Stress

Cited by 140 publications

References 13 publications

An Initial, Three-Day-Long Treatment with Alcohol Induces a Long-Lasting Phenomenon of Selective Tolerance in the Activity of the Rat Hypothalamic–Pituitary–Adrenal Axis

An Initial, Three-Day-Long Treatment with Alcohol Induces a Long-Lasting Phenomenon of Selective Tolerance in the Activity of the Rat Hypothalamic–Pituitary–Adrenal Axis

Illuminating the interrelated immune and endocrine adaptations after multiple exposures to short immobilization stress by in vivo blocking of IL-6

Dehydroepiandrosterone in relation to other adrenal hormones during an acute inflammatory stressful disease state compared with chronic inflammatory disease: role of interleukin-6 and tumour necrosis factor

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