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Titolo:
Paradoxical activational effects of a corticotropin-releasing factor-binding protein "ligand inhibitor" in rat brain
Autore:
Chan, RKW; Vale, WW; Sawchenko, PE;
Indirizzi:
Salk Inst Biol Studies, Neuronal Struct & Funct Lab, La Jolla, CA 92037 USA Salk Inst Biol Studies La Jolla CA USA 92037 Lab, La Jolla, CA 92037 USA Salk Inst Biol Studies, Clayton Fdn, Labs Peptide Biol, La Jolla, CA 92037USA Salk Inst Biol Studies La Jolla CA USA 92037 Biol, La Jolla, CA 92037USA
Titolo Testata:
NEUROSCIENCE
fascicolo: 1, volume: 101, anno: 2000,
pagine: 115 - 129
SICI:
0306-4522(2000)101:1<115:PAEOAC>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
CENTRAL-NERVOUS-SYSTEM; FACTOR-RECEPTOR; MESSENGER-RNAS; INSITU HYBRIDIZATION; HUMAN-PLASMA; WEIGHT-GAIN; HORMONE; EXPRESSION; PITUITARY; SECRETION;
Keywords:
Alzheimer's disease; corticotropin-releasing factor; CRF-binding protein; CRF receptors; c-fos; obesity;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Sawchenko, PE Salk Inst Biol Studies, Neuronal Struct & Funct Lab, 10010 NTorrey Pines Rd, La Jolla, CA 92037 USA Salk Inst Biol Studies 10010 N Torrey Pines Rd La Jolla CA USA 92037
Citazione:
R.K.W. Chan et al., "Paradoxical activational effects of a corticotropin-releasing factor-binding protein "ligand inhibitor" in rat brain", NEUROSCIENC, 101(1), 2000, pp. 115-129

Abstract

The corticotropin-releasing factor-binding protein is distinct from known corticotropin-releasing factor receptors, but can bind the peptide and neutralize its biological actions. Recent interest has centered about the therapeutic potential of "ligand inhibitors" of binding protein action, synthetic corticotropin-releasing factor fragments which are inactive at corticotropin-releasing factor receptors, but can displace the peptide from the binding protein, thereby increasing levels of free corticotropin-releasing factor. To identify sites of action of such ligands, the distribution of Fos expression seen following intracerebroventricular administration of rat/human corticotropin-releasing factor(6-33) (5-50 mug) was charted in relation to corticotropin-releasing factor-binding protein and receptor expression. It was expected that Fos induction would mimic aspects of the distribution of the two known corticotropin-releasing factor receptors, but the far greatercorrespondence was seen with that of the binding protein itself. This included neurons in the isocortex, the olfactory system, amygdala and a number of discrete brainstem cell groups; many Fos-immunoreactive neurons in each were found to co-express corticotropin-releasing factor-binding protein messenger RNA. Subsets of activated neurons co-expressed Type 1 corticotropin-releasing factor receptor messenger RNA, though these were largely limited to cell groups that also express the corticotropin-releasing factor-bindingprotein, and where binding protein immunoreactivity and Type 1 receptor transcripts were found to co-exist. Responsive neurons displaying Type 2 corticotropin-releasing factor receptor message were seen reliably only in the lateral septal nucleus. These findings support only a limited capacity of the ligand inhibitor to activate neurons bearing corticotropin-releasing factor receptors. The morepervasive activation seen among neurons that express the corticotropin-releasing factor-binding protein may be indicative of an unexpected role for this protein in signaling by corticotropin-releasing factor-related peptides. (C) 2000 IBRO. Published by Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/11/20 alle ore 00:37:18