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Titolo:
Persistent corticotropin-releasing factor, receptor desensitization and downregulation in the human neuroblastoma cell line IMR-32
Autore:
Roseboom, PH; Uban, CM; Kalin, NH;
Indirizzi:
Univ Wisconsin, Dept Psychiat, Madison, WI 53719 USA Univ Wisconsin Madison WI USA 53719 Dept Psychiat, Madison, WI 53719 USA Univ Wisconsin, Dept Pharmacol, Madison, WI 53719 USA Univ Wisconsin Madison WI USA 53719 Dept Pharmacol, Madison, WI 53719 USA Univ Wisconsin, Dept Psychol, Madison, WI 53719 USA Univ Wisconsin Madison WI USA 53719 , Dept Psychol, Madison, WI 53719 USA
Titolo Testata:
MOLECULAR BRAIN RESEARCH
fascicolo: 1-2, volume: 92, anno: 2001,
pagine: 115 - 127
SICI:
0169-328X(20010815)92:1-2<115:PCFRDA>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
MESSENGER-RIBONUCLEIC-ACID; PROTEIN-COUPLED RECEPTORS; RAT ANTERIOR-PITUITARY; FACTOR CRF; DIFFERENTIAL REGULATION; HOMOLOGOUS DESENSITIZATION; IMMOBILIZATION STRESS; RETINOBLASTOMA CELLS; BEHAVIORAL-RESPONSES; MATERNAL-DEPRIVATION;
Keywords:
resensitization; stress; sauvagine; adenylate cyclase; CRF41; receptor regulation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
60
Recensione:
Indirizzi per estratti:
Indirizzo: Roseboom, PH Univ Wisconsin, Dept Psychiat, 6001 Res Pk Blvd, Madison, WI 53719 USA Univ Wisconsin 6001 Res Pk Blvd Madison WI USA 53719 3719 USA
Citazione:
P.H. Roseboom et al., "Persistent corticotropin-releasing factor, receptor desensitization and downregulation in the human neuroblastoma cell line IMR-32", MOL BRAIN R, 92(1-2), 2001, pp. 115-127

Abstract

Brain corticotropin-releasing factor (CRF) systems integrate various responses to stress. Pathological responses to stress may result from errors in CRF receptor regulation in response to changes in synaptic CRF levels. To establish an in vitro model to study brain CRF receptors, we characterized the CRF-induced modulation of CRF1 receptors in the human neuroblastoma cellline, IMR-32. Treatment with CRF decreased CRF1 receptor binding and desensitized CRF-induced increases in cAMP. The decrease in binding had an EC50 of similar to 10 nM, was maximal by 30 min, and was blocked by the CRF receptor antagonist [D-Phe(12), Nle(21,38), C-alpha-MeLeu(37)]CRF12-41. The desensitization was homologous as vasoactive intestinal polypeptide-induced increases in cAMP were unchanged, and elevation of cAMP did not alter CRF1 receptor binding. Treatment with CRF for up to 24 h did not alter CRF1 receptor mRNA levels, suggesting that a posttranscriptional mechanism maintains the decrease in receptor binding. Interestingly, recovery of CRF receptor binding and CRF-stimulated cAMP production was only partial following exposure to 100 nM CRF. In contrast, receptor binding recovered to control levels following exposure to 10 nM CRF. These data suggest that exposure to high doses of CRF result in permanent changes characterized by only partial recovery. Identifying the mechanisms underlying this partial recovery may provide insights into mechanisms underlying the acute and chronic effects of stress on CRF receptor regulation. (C) 2001 Elsevier Science BY. All rights reserved.

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Documento generato il 10/08/20 alle ore 23:35:36