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Titolo:
Nociceptin/orphanin FQ exacerbates excitotoxic white-matter lesions in themurine neonatal brain
Autore:
Laudenbach, V; Calo, G; Guerrini, R; Lamboley, G; Benoist, JF; Evrard, P; Gressens, P;
Indirizzi:
Hop Robert Debre, Serv Neuropediat, INSERM E9935, F-75019 Paris, France Hop Robert Debre Paris France F-75019 NSERM E9935, F-75019 Paris, France Hop Robert Debre, Lab Biochim Hormonol, F-75019 Paris, France Hop Robert Debre Paris France F-75019 im Hormonol, F-75019 Paris, France Univ Ferrara, Dept Pharmaceut Sci, I-44100 Ferrara, Italy Univ Ferrara Ferrara Italy I-44100 harmaceut Sci, I-44100 Ferrara, Italy Univ Ferrara, Ctr Biotechnol, I-44100 Ferrara, Italy Univ Ferrara Ferrara Italy I-44100 tr Biotechnol, I-44100 Ferrara, Italy Univ Ferrara, Pharmacol Sect, Dept Expt & Clin Med, I-44100 Ferrara, ItalyUniv Ferrara Ferrara Italy I-44100 pt & Clin Med, I-44100 Ferrara, Italy
Titolo Testata:
JOURNAL OF CLINICAL INVESTIGATION
fascicolo: 4, volume: 107, anno: 2001,
pagine: 457 - 466
SICI:
0021-9738(200102)107:4<457:NFEEWL>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASOACTIVE-INTESTINAL-PEPTIDE; ORPHAN OPIOID RECEPTOR; CENTRAL-NERVOUS-SYSTEM; NEUROBLASTOMA-CELLS; GENE-EXPRESSION; CEREBRAL-PALSY; RISK-FACTORS; IN-VITRO; ANTAGONIST; RAT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Gressens, P Hop Robert Debre, Serv Neuropediat, INSERM E9935, 48 Blvd Serurier, F-75019 Paris, France Hop Robert Debre 48 Blvd Serurier Paris FranceF-75019 France
Citazione:
V. Laudenbach et al., "Nociceptin/orphanin FQ exacerbates excitotoxic white-matter lesions in themurine neonatal brain", J CLIN INV, 107(4), 2001, pp. 457-466

Abstract

Intracerebral administration of the excitotoxin ibotenate to newborn mice induces white-matter lesions, mimicking brain lesions that occur in human preterm infants. Nociceptin (NC), also called orphanin FQ, is the endogenousligand of the opioid receptor-like 1 (ORL1) receptor and does not: bind classical high-affinity opioid receptors, In the present study, administration of NC exacerbated ibotenate-induced white-matter lesions while coadministration of ibotenate with either of two NC antagonists reduced excitotoxic white-matter lesions by up to 64%. Neither ibotenate plus endomorphin I (a selective mu receptor agonist), nor ibotenate plus naloxone (a classical opioid receptor antagonist) modulated the excitotoxic lesion. Pretreatment with antisense oligonucleotides targeting the NC precursor peptide mRNA significantly reduced ibotenate-induced white-matter damage. Finally, high doses of fentanyl, which stimulates both classical mu opioid receptors and ORL1, exacerbated excitotoxic white-matter lesion. This toxic effect was blocked by inhibiting ORL1 but not classical opioid receptors. Together, these findings show that endogenous or exogenous stimulation of the ORL1 receptor canbe neurotoxic and that blocking NC signaling protects the white matter against excitotoxic challenge. These data point to potential new avenues for neuroprotection in human preterm infants at high risk of brain lesions.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 08:35:39