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Titolo:
Paraquat elicited neurobehavioral syndrome caused by dopaminergic neuron loss
Autore:
Brooks, AI; Chadwick, CA; Gelbard, HA; Cory-Slechta, DA; Federoff, HJ;
Indirizzi:
Univr,ochester, Sch Med & Dent, Div Mol Med, Ctr Aging & Dev Biol, Rocheste Univ Rochester Rochester NY USA 14642 Med, Ctr Aging & Dev Biol, Rocheste Univ Rochester, Sch Med & Dent, Dept Immunol, Rochester, NY 14642 USA UnivRochester Rochester NY USA 14642 pt Immunol, Rochester, NY 14642 USA Univ Rochester, Sch Med & Dent, Dept Neurol, Rochester, NY 14642 USA Univ Rochester Rochester NY USA 14642 ept Neurol, Rochester, NY 14642 USA Univ Rochester, Sch Med & Dent, Dept Environm Med, Rochester, NY 14642 USAUniv Rochester Rochester NY USA 14642 vironm Med, Rochester, NY 14642 USA Univ Rochester, Sch Med & Dent, Dept Microbiol, Rochester, NY 14642 USA Univ Rochester Rochester NY USA 14642 Microbiol, Rochester, NY 14642 USA
Titolo Testata:
BRAIN RESEARCH
fascicolo: 1-2, volume: 823, anno: 1999,
pagine: 1 - 10
SICI:
0006-8993(19990327)823:1-2<1:PENSCB>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
PARKINSONISM-INDUCING NEUROTOXIN; MPTP-INDUCED NEUROTOXICITY; C57/B1 MICE; WEIGHT-LOSS; DISEASE; RAT; BRAIN; SYSTEM; N-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE; EPIDEMIOLOGY;
Keywords:
Parkinson's; MPTP; paraquat; tyrosine hydroxylase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Federoff, HJ Univ601chester, Sch Med & Dent, Div Mol Med, Ctr Aging & Dev Biol, Box 645, Univ Rochester Box 645,601 Elmwood Ave Rochester NY USA 14642
Citazione:
A.I. Brooks et al., "Paraquat elicited neurobehavioral syndrome caused by dopaminergic neuron loss", BRAIN RES, 823(1-2), 1999, pp. 1-10

Abstract

The herbicide paraquat, bearing structural similarity to the known dopaminergic neurotoxicant MPTP, has been suggested as a potential etiologic factor in Parkinson's disease. Consideration of paraquat as a candidate neurotoxicant requires demonstration that systemic delivery produces substantia nigra dopaminergic neuron loss and the attendant neurobehavioral syndrome reflecting depletion of dopamine terminals within the striatum. To address these issues paraquat was administered systemically into adult C57 b1/6 mice, ambulatory behavior monitored, substantia nigra dopamine neuron number and striatal dopamine terminal density quantified. The data indicate that paraquat like MPTP elicits a dose-dependent decrease in substantia nigra dopaminergic neurons assessed by a Fluoro-gold prelabeling method, a decline in striatal dopamine nerve terminal density assessed by measurement of tyrosine hydroxylase immunoreactivity; and neurobehavioral syndrome characterized by reduced ambulatory activity. Taken together, these data suggest that systemically absorbed paraquat crosses the blood-brain barrier to cause destruction of dopamine neurons in the substantia nigra, consequent reduction of dopaminergic innervation of the striatum and a neurobehavioral syndrome similar to the well characterized and bona fide dopaminergic toxin MPTP. (C) 1999Elsevier Science B.V. All rights reserved.

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Documento generato il 03/07/20 alle ore 01:38:52