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

Hdl Handle:
http://hdl.handle.net/10147/209117
Title:
The stress response and the hypothalamic-pituitary-adrenal axis: from molecule to melancholia.
Authors:
O'Connor, T M; O'Halloran, D J; Shanahan, F
Affiliation:
Department of Endocrinology and Medicine, Cork University Hospital and University, College Cork, Cork, Ireland. terryoconnor@eircom.net
Citation:
QJM. 2000 Jun;93(6):323-33.
Journal:
QJM : monthly journal of the Association of Physicians
Issue Date:
3-Feb-2012
URI:
http://hdl.handle.net/10147/209117
PubMed ID:
10873181
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-alpha. 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.
Language:
eng
MeSH:
Animals; Arthritis, Rheumatoid/physiopathology; Depressive Disorder/physiopathology; Gene Expression/physiology; Glucocorticoids/physiology; Humans; Hypothalamo-Hypophyseal System/*physiology; Interleukin-1/physiology; Interleukin-6/physiology; Pituitary-Adrenal System/*physiology; Protein Biosynthesis/physiology; Rats; Rats, Inbred Lew; Stress, Physiological/*physiopathology; Transcription, Genetic/physiology; Tumor Necrosis Factor-alpha/physiology
ISSN:
1460-2725 (Print); 1460-2393 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorO'Connor, T Men_GB
dc.contributor.authorO'Halloran, D Jen_GB
dc.contributor.authorShanahan, Fen_GB
dc.date.accessioned2012-02-03T15:12:43Z-
dc.date.available2012-02-03T15:12:43Z-
dc.date.issued2012-02-03T15:12:43Z-
dc.identifier.citationQJM. 2000 Jun;93(6):323-33.en_GB
dc.identifier.issn1460-2725 (Print)en_GB
dc.identifier.issn1460-2393 (Linking)en_GB
dc.identifier.pmid10873181en_GB
dc.identifier.urihttp://hdl.handle.net/10147/209117-
dc.description.abstractOrganisms 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-alpha. 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.en_GB
dc.language.isoengen_GB
dc.subject.meshAnimalsen_GB
dc.subject.meshArthritis, Rheumatoid/physiopathologyen_GB
dc.subject.meshDepressive Disorder/physiopathologyen_GB
dc.subject.meshGene Expression/physiologyen_GB
dc.subject.meshGlucocorticoids/physiologyen_GB
dc.subject.meshHumansen_GB
dc.subject.meshHypothalamo-Hypophyseal System/*physiologyen_GB
dc.subject.meshInterleukin-1/physiologyen_GB
dc.subject.meshInterleukin-6/physiologyen_GB
dc.subject.meshPituitary-Adrenal System/*physiologyen_GB
dc.subject.meshProtein Biosynthesis/physiologyen_GB
dc.subject.meshRatsen_GB
dc.subject.meshRats, Inbred Lewen_GB
dc.subject.meshStress, Physiological/*physiopathologyen_GB
dc.subject.meshTranscription, Genetic/physiologyen_GB
dc.subject.meshTumor Necrosis Factor-alpha/physiologyen_GB
dc.titleThe stress response and the hypothalamic-pituitary-adrenal axis: from molecule to melancholia.en_GB
dc.contributor.departmentDepartment of Endocrinology and Medicine, Cork University Hospital and University, College Cork, Cork, Ireland. terryoconnor@eircom.neten_GB
dc.identifier.journalQJM : monthly journal of the Association of Physiciansen_GB
dc.description.provinceMunster-

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