Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Nicotine-induced excitation of locus coeruleus neurons is blocked by elevated levels of endogenous kynurenic acid
Autore:
Erhardt, S; Hajos, M; Lindberg, A; Engberg, G;
Indirizzi:
Karolinska Inst, Dept Physiol & Pharmacol, SE-17177 Stockholm, Sweden Karolinska Inst Stockholm Sweden SE-17177 ol, SE-17177 Stockholm, Sweden Univ Oxford, Radcliffe Infirm, Dept Clin Pharmacol, Oxford OX1 2JD, England Univ Oxford Oxford England OX1 2JD in Pharmacol, Oxford OX1 2JD, England
Titolo Testata:
SYNAPSE
fascicolo: 2, volume: 37, anno: 2000,
pagine: 104 - 108
SICI:
0887-4476(200008)37:2<104:NEOLCN>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
NUCLEUS PARAGIGANTOCELLULARIS; MAMMALIAN BRAIN; PERFORMANCE; INHIBITION; ACTIVATION; ANTAGONIST; CERULEUS; RELEASE; INPUT; RATS;
Keywords:
PNU 156561A; noradrenaline; glutamate;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
22
Recensione:
Indirizzi per estratti:
Indirizzo: Erhardt, S Karolinska Inst, Dept Physiol & Pharmacol, SE-17177 Stockholm, Sweden Karolinska Inst Stockholm Sweden SE-17177 7 Stockholm, Sweden
Citazione:
S. Erhardt et al., "Nicotine-induced excitation of locus coeruleus neurons is blocked by elevated levels of endogenous kynurenic acid", SYNAPSE, 37(2), 2000, pp. 104-108

Abstract

The present electrophysiological study shows that manipulation with endogenous brain kynurenic acid (KYNA) is able to affect the response of central noradrenergic neurons to nicotine. Previous studies have shown that systemically administered nicotine in low doses is associated with a marked, but short-lasting increase in the firing rate of rat noradrenergic neurons in the locus coeruleus (LC). This action of nicotine is of peripheral origin andfinally mediated via a release of glutamate within the LC. KYNA is an endogenous glutamate receptor antagonist, which shows an uneven distribution inhuman brain. Previous studies have shown that a potent inhibitor of kynurenine 3-hydroxylase, PNU 156561A, is able to dose-dependently increase the levels of KYNA in brain. Anesthetized rats were given PNU 156561A in a dose that caused a 5-fold increase in brain KYNA levels after 3-6 hours (40 mg/kg, i.v.). This treatment was found to abolish the increase in firing rate of LC neurons induced by nicotine (25-200 mu g/kg, i.v.). The results of thepresent study show that an increased concentration of endogenous brain KYNA is able to inhibit the activation of central noradrenergic neurons by nicotine. In addition, our results highlight the role of endogenous KYNA in brain as a potentially important modulator of brain glutamatergic responses. Synapse 37:104-108, 2000. (C) 2000 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 08:36:34