Glucocorticoid inhibition of stress-induced changes in hypothalamic corticotrophin-releasing factor messenger RNA and proenkephalin A messenger RNA.
We have examined the effects of localised administration of the synthetic glucocorticoid dexamethasone on basal and stress-induced levels of mRNA for both corticotrophin-releasing factor (CRF) and proenkephalin A, in parvocellular neurons of the paraventricular nucleus (PVN). Unilateral implants of cholesterol directly over the PVN had no effect on either basal or stress-induced increase of CRF and proenkephalin A message. However, unilateral implants of dexamethasone significantly decreased basal CRF mRNA compared to the contralateral, unimplanted side and prevented the increase in CRF and proenkephalin A mRNA 4 hours after ip hypertonic saline stress. These findings confirm the PVN as a site for glucocorticoid feedback. Furthermore the data demonstrates a steroid-sensitive stress mediated increase in proenkephalin A mRNA which provides additional evidence for a role of the endogenous opiates in the hypothalamic neuroendocrine response to stress.
Harbuz
M S
MS
Medical Unit, Charing Cross and Westminster Hospital Medical School, Westminster Hospital, London, UK.
Lightman
S L
SL
D000818:Animals; D003346:Corticotropin-Releasing Hormone / Q000235:genetics*; D003907:Dexamethasone / Q000494:pharmacology*; D004745:Enkephalins / Q000235:genetics*; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism*; D011498:Protein Precursors / Q000235:genetics*; D012333:RNA, Messenger / Q000096:biosynthesis*; D051381:Rats; D011919:Rats, Inbred Strains; D013312:Stress, Physiological / Q000378:metabolism
D004745:Enkephalins; D011498:Protein Precursors; D012333:RNA, Messenger; C029992:proenkephalin; D003907:Dexamethasone; D003346:Corticotropin-Releasing Hormone