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Titolo:
Increased dopamine uptake in striatal synaptosomes after treatment of ratswith amantadine
Autore:
Page, G; Peeters, M; Maloteaux, JM; Hermans, E;
Indirizzi:
Univ Catholique Louvain, Pharmacol Lab, B-1200 Brussels, Belgium Univ Catholique Louvain Brussels Belgium B-1200 B-1200 Brussels, Belgium
Titolo Testata:
EUROPEAN JOURNAL OF PHARMACOLOGY
fascicolo: 1-2, volume: 403, anno: 2000,
pagine: 75 - 80
SICI:
0014-2999(20000901)403:1-2<75:IDUISS>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
IN-VIVO; TRANSPORTER; BRAIN; NMDA; BINDING; RELEASE; PHENCYCLIDINE; MK-801; NORADRENALINE; ANTAGONISM;
Keywords:
glutamate; dopamine uptake; Parkinson's disease; NMDA receptor;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Page, G Univ Catholique Louvain, Pharmacol Lab, FARL 54 10,Ave Hippocrate 54, B-1200 Brussels, Belgium Univ Catholique Louvain FARL 54 10,Ave Hippocrate 54 Brussels Belgium B-1200
Citazione:
G. Page et al., "Increased dopamine uptake in striatal synaptosomes after treatment of ratswith amantadine", EUR J PHARM, 403(1-2), 2000, pp. 75-80

Abstract

The aim of the present study was to investigate the effect of short- and long-term treatments with amantadine on the activity of the neuronal dopamine transporter (DAT) in the rat striatum. For this purpose, the [H-3]dopamine uptake was measured in striatal synaptosomes prepared from rats treated for 2, 7 and 14 days with amantadine (40 mg/kg; i.p.). After 7 days of treatment, amantadine increased the apparent V-max by 30% without modification of the apparent K-m of dopamine uptake whereas no change in these parameterswas observed after 2 and 14 days treatment. Binding assays conducted with [H-3]GBR-12935 on membranes prepared from animals treated with amantadine revealed no difference in the density and the affinity of striatal DAT binding sites as compared to control. This indicates that the increased dopamineuptake was not reflecting a modification at the level of the DAT expression. The activity of the DAT is regulated by phosphorylation and one may propose that ionotropic glutamate receptors present on presynaptic terminals directly modulate this phosphorylation. An indirect mechanism would involve presynaptic dopamine receptors that control the activity of the DAT in response to the increased dopamine concentration in the synaptic cleft. (C) 2000Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/09/20 alle ore 12:53:54