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Titolo:
Sibutramine does not decrease the number of 5-HT re-uptake sites in rat brain and, like fluoxetine, protects against the deficits produced by dexfenfluramine
Autore:
Cheetham, SC; Viggers, JA; Slater, NA; Heal, DJ;
Indirizzi:
BASF Pharma, Res & Dev, Nottingham NG1 1GF, England BASF Pharma Nottingham England NG1 1GF Dev, Nottingham NG1 1GF, England
Titolo Testata:
NEUROPHARMACOLOGY
fascicolo: 11, volume: 39, anno: 2000,
pagine: 2028 - 2035
SICI:
0028-3908(2000)39:11<2028:SDNDTN>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
H-3 PAROXETINE BINDING; MONOAMINE REUPTAKE INHIBITORS; D-FENFLURAMINE; DOWN-REGULATION; 5-HYDROXYTRYPTAMINE RELEASE; ANTIDEPRESSANT TREATMENTS; SEROTONIN NEUROTOXICITY; PARA-CHLOROAMPHETAMINE; HYDROCHLORIDE; MECHANISM;
Keywords:
[H-3]paroxetine binding; 5-HT re-uptake sites; sibutramine; fluoxetine; dexfenfluramine; rat brain;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Cheetham, SC BASF Pharma, Res & Dev, Nottingham NG1 1GF, England BASF Pharma Nottingham England NG1 1GF ham NG1 1GF, England
Citazione:
S.C. Cheetham et al., "Sibutramine does not decrease the number of 5-HT re-uptake sites in rat brain and, like fluoxetine, protects against the deficits produced by dexfenfluramine", NEUROPHARM, 39(11), 2000, pp. 2028-2035

Abstract

The effect of sibutramine and dexfenfluramine on 5-HT re-uptake sites, labelled with [H-3]paroxetine, have been determined in various rat brain regions. In addition, the ability of fluoxetine and sibutramine to protect against the changes in [3H]paroxetine binding produced by dexfenfluramine was examined. Sibutramine (9 mg/kg, p.o.) and dexfenfluramine (1, 3 and 10 mg/kg,p.o.) were administered twice daily (before 09.00 h and after 16.00 h) forfour days, followed by a 14 day drug-free period. In the protection studies, fluoxetine (10 mg/kg, i.p.) and sibutramine (9 mg/kg, p.o.) were given 1h prior to dexfenfluramine (10 mg/kg, p.o.) using the same dosing regimen as described above. Sibutramine (9 mg/kg, p.o.; three times its ED50 to inhibit food intake at 2 h) had no significant effect on the number or affinity of 5-HT re-uptake sites the brain regions studied. In contrast, dexfenfluramine at an equivalent dose (3 mg/kg, p.o.) significantly decreased the number of 5-HT re-uptake sites in frontal cortex (by 35%), hippocampus (by 47%) and hypothalamus (by 27%). This effect was dose-dependent with marked decreases (by 58-84%) in the number of sites following 10 mg/kg, p.o. These effects were not associated with changes in binding affinity. Fluoxetine (10mg/kg, i.p.) completely blocked the effect of dexfenfluramine (10 mg/kg, p.o.) without having any significant effect alone. Sibutramine (9 mg/kg, p.o.) also blocked the effects of dexfenfluramine, although the reversal was only partial in frontal cortex, hippocampus and hypothalamus. Thus sibutramine, unlike dexfenfluramine, does not alter brain 5-HT re-uptake sites. Furthermore, sibutramine and fluoxetine protect against the deficits in 5-HT re-uptake sites produced by dexfenfluramine. These data provide further evidence that sibutramine is a 5-HT re-uptake inhibitor and it does not have neurotoxic potential. (C) 2000 Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 09:09:30