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Expression of Corticotropin‐Releasing Factor mRNA in Response to Stress

2007; Wiley; Linguagem: Inglês

10.1002/9780470514368.ch9

1935-4657

Stafford L. Lightman, Michael S. Harbuz,

Neuroendocrine regulation and behavior

Expression of Corticotropin-Releasing Factor mRNA in Response to Stress Stafford L. Lightman, Stafford L. Lightman Neuroendocrinology Unit, Charing Cross & Westminster Medical School, Charing Cross Hospital, Fulham Palace Road, London W6 8RF, UKSearch for more papers by this authorMichael S. Harbuz, Michael S. Harbuz Neuroendocrinology Unit, Charing Cross & Westminster Medical School, Charing Cross Hospital, Fulham Palace Road, London W6 8RF, UKSearch for more papers by this author Stafford L. Lightman, Stafford L. Lightman Neuroendocrinology Unit, Charing Cross & Westminster Medical School, Charing Cross Hospital, Fulham Palace Road, London W6 8RF, UKSearch for more papers by this authorMichael S. Harbuz, Michael S. Harbuz Neuroendocrinology Unit, Charing Cross & Westminster Medical School, Charing Cross Hospital, Fulham Palace Road, London W6 8RF, UKSearch for more papers by this author Book Editor(s):Derek J. Chadwick, Derek J. Chadwick OrganizerSearch for more papers by this authorJoan Marsh, Joan Marsh OrganizerSearch for more papers by this authorKate Ackrill, Kate AckrillSearch for more papers by this author First published: 28 September 2007 https://doi.org/10.1002/9780470514368.ch9Citations: 10Book Series:Novartis Foundation Symposia AboutPDFPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShareShare a linkShare onEmailFacebookTwitterLinkedInRedditWechat Summary The corticotropin-releasing factor (CRF)-containing neurons of the parvo-cellular division of the hypothalamic paraventricular nucleus play a pivotal role in the regulation of the hypothalamo-pituitary-adrenal axis. We have studied the regulation of these neurons in the conscious rat using the technique of quantitative in situ hybridization histochemistry. Corticosteroid feedback reduces CRF mRNA levels in a dose-dependent manner, although even prolonged administration of very high doses cannot abolish CRF transcripts completely. Both physical and psychological stressors produce a robust and readily reproducible increase in CRF mRNA. These responses cannot be prevented by changes in circulating corticosteroids—a similar magnitude of response occurs with high basal levels in the adrenalectomized animal and with low basal levels during treatment with supraphysiological doses of glucocorticoid. Alterations in CRF mRNA levels in response to stress are, however, lost during the physiological condition of lactation, a state known to result in stress hyporesponsiveness, and also after 6-hydroxydopamine lesions to the catecholaminergic innervation of the paraventricular nucleus. We have also studied two conditions of chronic immunological activation of the hypothalamo-pituitary-adrenal axis—adjuvant-induced arthritis and experimental allergic encephalomyelitis. Both of these result in activation of the hypothalamo-pituitary-adrenal axis with increased plasma corticosterone and ACTH, and pituitary pro-opiomelanocortin (POMC) mRNA. Unexpectedly, however, the activation of pituitary corticotrophs does not seem to be a primary result of increased activation of the CRF neurons, which actually show a consistent fall in CRF mRNA. References Abe K, Critchlow V 1977 Effects of corticosterone, dexamethasone and surgical isolation of medial basal hypothalamus on rapid feedback control of stress-induced corticotropin secretion in female rats. Endocrinology 101: 498–505 10.1210/endo-101-2-498 CASPubMedWeb of Science®Google Scholar Aguilera G, Lightman SL, Kiss A 1992 Role of the magnocellular system (MCS) in pituitary ACTH responses. 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