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Titolo:
COMPARISON OF KEY STEPS IN 1-METHYL-4-PHENYL-1,2,4,6-TETRAHYDROPYRIDINE (MPTP) NEUROTOXICITY IN RODENTS
Autore:
SUNDSTROM E; SAMUELSSON EB;
Indirizzi:
KFC NOVUM,DIV GERIATR MED S-14186 HUDDINGE SWEDEN HUDDINGE UNIV HOSP,KAROLINSKA INST,DIV GERIATR MED,KFC NOVUM S-14186 HUDDINGE SWEDEN
Titolo Testata:
Pharmacology & toxicology
fascicolo: 5, volume: 81, anno: 1997,
pagine: 226 - 231
SICI:
0901-9928(1997)81:5<226:COKSI1>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
CENTRAL CATECHOLAMINE NEURONS; DOPAMINERGIC NEUROTOXIN; MONOAMINE-OXIDASE; 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE MPTP; CHRONIC PARKINSONISM; SPECIES SENSITIVITY; 1-METHYL-4-PHENYLPYRIDINIUM; METABOLITE; MICE; INHIBITION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
28
Recensione:
Indirizzi per estratti:
Citazione:
E. Sundstrom e E.B. Samuelsson, "COMPARISON OF KEY STEPS IN 1-METHYL-4-PHENYL-1,2,4,6-TETRAHYDROPYRIDINE (MPTP) NEUROTOXICITY IN RODENTS", Pharmacology & toxicology, 81(5), 1997, pp. 226-231

Abstract

Three steps in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity were compared with the neurodegenerative effects of the toxin in mice and rats. Firstly we compared the neurotoxicity of MPTP, mediated by monoamine oxidase (MAO)-B, to that of hyl-4-(2'-methylphenyl)-1,2,3,6-tetrahydropyridine (2'-CH3-MPTP), an analogue oxidized by MAO-A and MAO-B. Both toxins caused degeneration of dopamine terminals in mice but not in rats. In NMRI mice noradrenaline terminals were also affected by both toxins. Pretreatment with deprenyl to prevent MAO-B-mediated oxidation in the capillary endothelium enhanced dopamine toxicity to 2'-CH3-MPTP in nucleus accumbens but no potentiation was seenin striatum and the olfactory tubercle. Secondly, synaptosomal uptakeof the 1-methyl-4-phenylpyridinium ion (MPP+) was studied. Uptake in rats was not significantly different from that in the two mice strains. Thirdly, no significant differences were found in MPP+-induced lactate production in striatal slices or synaptosomes. We conclude that thelack of effect of MPTP in rats is not due to mechanisms specific for MPTP but probably to the ability of rat catecholamine neurons to cope with, and survive, impaired energy metabolism.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 23:42:37