Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Modulation of 5-hydroxytryptamine efflux from rat cortical synaptosomes byopioids and nociceptin
Autore:
Sbrenna, S; Marti, M; Morari, M; Calo, G; Guerrini, R; Beani, L; Bianchi, C;
Indirizzi:
Univ Ferrara, Dept Expt & Clin Med, Pharmacol Sect, I-44100 Ferrara, ItalyUniv Ferrara Ferrara Italy I-44100 harmacol Sect, I-44100 Ferrara, Italy Univ Ferrara, Dept Pharmaceut Sci, I-44100 Ferrara, Italy Univ Ferrara Ferrara Italy I-44100 harmaceut Sci, I-44100 Ferrara, Italy
Titolo Testata:
BRITISH JOURNAL OF PHARMACOLOGY
fascicolo: 2, volume: 130, anno: 2000,
pagine: 425 - 433
SICI:
0007-1188(200005)130:2<425:MO5EFR>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
NALOXONE BENZOYLHYDRAZONE; NORADRENALINE RELEASE; RECEPTOR ANTAGONIST; INTERNATIONAL UNION; ENDOGENOUS AGONIST; GLUTAMATE RELEASE; ORL1 RECEPTORS; BRAIN CORTEX; MU; KAPPA;
Keywords:
synaptosomes; opioid receptors; nociceptin; 5-hydroxytryptamine; rat cerebral cortex; ORL1; [Phe(1 psi)(CH2NH)Gly(2)]NC(1-13)NH2; [Nphe(1)]NC(1-13)NH2;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Morari, M Univ Ferrara, Dept Expt & Clin Med, Pharmacol Sect, Via Fossato Mortara 17-19, I-44100 Ferrara, Italy Univ Ferrara Via Fossato Mortara 17-19 Ferrara Italy I-44100 ly
Citazione:
S. Sbrenna et al., "Modulation of 5-hydroxytryptamine efflux from rat cortical synaptosomes byopioids and nociceptin", BR J PHARM, 130(2), 2000, pp. 425-433

Abstract

1 The modulation of [H-3]-5-hydroxytryptamine ([H-3]-5-HT) efflux from superfused rat cortical synaptosomes by delta, kappa, mu and ORL1 opioid receptor agonists and antagonists was studied.2 Spontaneous [H-3]-5-HT efflux was reduced (20% inhibition) by either 0.5mu M tetrodotoxin or Ca2+-omission. Ten mM K+-evoked [H-3]-5-HT overflow was largely Ca2+-dependent (90%) and tetrodotoxin-sensitive (50%).3 The delta receptor agonist, deltorphin-I, failed to modulate the K+-evoked neurotransmitter efflux up to 0.3 mu M. The kappa and the mu receptor agonists, U-50,488 and endomorphin-1, inhibited K+-evoked [H-3]-5-HT overflow(EC50=112 and 7 nM, respectively; E-max=28 and 29% inhibition, respectively) in a norBinaltorphimine- (0.3 mu M) and naloxone- (1 mu M) sensitive manner, respectively. None of these agonists significantly affected spontaneous [H-3]-5-HT efflux.4 The ORL1 receptor agonist nociceptin inhibited both spontaneous (EC50=67nM) and K+-evoked (EC50=13 nM; E-max=52% inhibition) [H-3]-5-HT efflux. The effect of NC was insensitive to naloxone (up to 10 mu M), but was antagonized by [Nphe(1)]nociceptin(1-13)NH2 (a novel selective ORL1 receptor antagonist; pA(2)=6.7) and by naloxone benzoylhydrazone (pA(2)=6.3). The ORL1 ligand [Phe(1)phi(CH2-NH)Gly(2)]nociceptin(1-13)NH2 also inhibited K+ stimulated [H-3]-5-HT overflow (EC50=64nM; E-max=31% inhibition), but its effect was partially antagonized by 10 mu M naloxone.5 It is concluded that the ORL1 receptor is the most important presynapticmodulator of neocortical 5-HT release within the opioid receptor family. This suggests that the ORL1/nociceptin system may have a powerful role in the control of cerebral 5-MT-mediated biological functions.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/07/20 alle ore 15:00:07