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

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    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
    Issue Date
    2012-02-03T15:12:43Z
    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
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    Citation
    QJM. 2000 Jun;93(6):323-33.
    Journal
    QJM : monthly journal of the Association of Physicians
    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
    ISSN
    1460-2725 (Print)
    1460-2393 (Linking)
    Collections
    Cork University Hospital

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