The stress response and the hypothalamic‐pituitary‐adrenal axis: from molecule to melancholia

The stress response and the hypothalamic‐pituitary‐adrenal axis: from molecule to melancholia Organisms survive by maintaining equilibrium with their environment. The stress system is critical to this homeostasis. Glucocorticoids modulate the stress response at a molecular level by altering gene expression, transcription, and translation, among other pathways. The effect is the inhibition of the functions of inflammatory cells, predominantly mediated through inhibition of cytokines, such as IL‐1, IL‐6, and TNF‐ α . The central effectors of the stress response are the corticotrophin‐releasing hormone (CRH) and locus coeruleus‐norepinephrine (LC‐NE)/sympathetic systems. The CRH system activates the stress response and is subject to modulation by cytokines, hormones, and neurotransmitters. Glucocorticoids also modulate the growth, reproductive and thyroid axes. Abnormalities of stress system activation have been shown in inflammatory diseases such as rheumatoid arthritis, as well as behavioural syndromes such as melancholic depression. These disorders are comparable to those seen in rats whose CRH system is genetically abnormal. Thus, the stress response is central to resistance to inflammatory and behavioural syndromes. In this review, we describe the response to stress at molecular, cellular, neuroendocrine and behavioural levels, and discuss the disease processes that result from a dysregulation of this response, as well as recent developments in their treatment. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png QJM: An International Journal of Medicine Oxford University Press

The stress response and the hypothalamic‐pituitary‐adrenal axis: from molecule to melancholia

The stress response and the hypothalamic‐pituitary‐adrenal axis: from molecule to melancholia


Q J Med 2000; 93:323­333 Review QJM T.M. O'CONNOR, D.J. O'HALLORAN and F. SHANAHAN From the Departments of Endocrinology and Medicine, Cork University Hospital and University College Cork, Cork, Ireland Summary Organisms survive by maintaining equilibrium with their environment. The stress system is critical to this homeostasis. Glucocorticoids modulate at a molecular level by altering gene expression, transcription, and translation, among other pathways. The effect is the inhibition of the functions of inflammatory cells, predominantly mediated through inhibition of cytokines, such as IL-1, IL-6, and TNF-a. The central effectors of are the corticotrophin-releasing hormone (CRH) and locus coeruleus-norepinephrine (LC-NE)/sympathetic systems. The CRH system activates and is subject to modulation by cytokines, hormones, and neurotransmitters. Glucocorticoids also modulate the growth, reproductive and thyroid axes. Abnormalities of stress system activation have been shown in inflammatory diseases such as rheumatoid arthritis, as well as behavioural syndromes such as melancholic depression. These disorders are comparable to those seen in rats whose CRH system is genetically abnormal. Thus, is central to resistance to inflammatory and behavioural syndromes. In this review, we describe the response to stress at molecular, cellular, neuroendocrine and behavioural levels, and discuss the disease processes that result from a dysregulation of this response, as well as recent developments in their treatment. Introduction Organisms survive by maintaining a dynamic equilibrium with their environment. The organization of this homeostasis exists at molecular, cellular, physiological and behavioural levels. Stress is a state of threat to this equilibrium, and adaptation to stress, or allostasis, confers a survival advantage. Successful adaptation requires not only the ability to respond to stress, but also the ability to control appropriately. This stress system...
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Publisher
Oxford University Press
Copyright
Copyright 2000
ISSN
1460-2725
eISSN
1460-2393
D.O.I.
10.1093/qjmed/93.6.323
Publisher site
See Article on Publisher Site

Abstract

Organisms survive by maintaining equilibrium with their environment. The stress system is critical to this homeostasis. Glucocorticoids modulate the stress response at a molecular level by altering gene expression, transcription, and translation, among other pathways. The effect is the inhibition of the functions of inflammatory cells, predominantly mediated through inhibition of cytokines, such as IL‐1, IL‐6, and TNF‐ α . The central effectors of the stress response are the corticotrophin‐releasing hormone (CRH) and locus coeruleus‐norepinephrine (LC‐NE)/sympathetic systems. The CRH system activates the stress response and is subject to modulation by cytokines, hormones, and neurotransmitters. Glucocorticoids also modulate the growth, reproductive and thyroid axes. Abnormalities of stress system activation have been shown in inflammatory diseases such as rheumatoid arthritis, as well as behavioural syndromes such as melancholic depression. These disorders are comparable to those seen in rats whose CRH system is genetically abnormal. Thus, the stress response is central to resistance to inflammatory and behavioural syndromes. In this review, we describe the response to stress at molecular, cellular, neuroendocrine and behavioural levels, and discuss the disease processes that result from a dysregulation of this response, as well as recent developments in their treatment.

Journal

QJM: An International Journal of MedicineOxford University Press

Published: Jun 1, 2000

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