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Titolo:
GDNF reverses priming for dyskinesia in MPTP-treated, L-DOPA-primed commonmarmosets
Autore:
Iravani, MM; Costa, S; Jackson, MJ; Tel, BC; Cannizzaro, C; Pearce, RKB; Jenner, P;
Indirizzi:
Univ London Kings Coll, Guys Kings & St Thomas Sch Biomed Sci, Neurodegenerat Dis Res Ctr, London SE1 1UL, England Univ London Kings Coll London England SE1 1UL r, London SE1 1UL, England
Titolo Testata:
EUROPEAN JOURNAL OF NEUROSCIENCE
fascicolo: 3, volume: 13, anno: 2001,
pagine: 597 - 608
SICI:
0953-816X(200102)13:3<597:GRPFDI>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
LEVODOPA-INDUCED DYSKINESIAS; NIGRAL DOPAMINERGIC-NEURONS; BOLUS INTRAVENTRICULAR-INJECTION; 6-HYDROXYDOPAMINE IN-VIVO; NEUROTROPHIC FACTOR GDNF; CELL-LINE; PARKINSONS-DISEASE; GENE-EXPRESSION; SUBSTANTIA-NIGRA; GROWTH-FACTOR;
Keywords:
dyskinesia; glial cell line-derived neurotrophic factor; L-DOPA; marmoset; MPTP; Parkinson's disease;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Jenner, P Univ London Kings Coll, Guys Kings & St Thomas Sch Biomed Sci, Neurodegenerat Dis Res Ctr, London SE1 1UL, England Univ London Kings Coll London England SE1 1UL SE1 1UL, England
Citazione:
M.M. Iravani et al., "GDNF reverses priming for dyskinesia in MPTP-treated, L-DOPA-primed commonmarmosets", EUR J NEURO, 13(3), 2001, pp. 597-608

Abstract

Parkinson's disease (PD) is associated with a progressive loss of dopamineneurons in the substantia nigra and degeneration of dopaminergic terminalsin the striatum. Although L-DOPA treatment provides the most effective symptomatic relief for PD it does not prevent the progression of the disease, and its long-term use is associated with the onset of dyskinesia. In rodentand primate studies, glial cell line-derived neurotrophic factor (GDNF) may prevent 6-OHDA- or MPTP-induced nigral degeneration and so may be beneficial in the treatment of PD. In this study, we investigate the effects of GDNF on the expression of dyskinesia in L-DOPA-primed MPTP-treated common marmosets, exhibiting dyskinesia. GDNF or saline was administered by two intraventricular injections, 4 weeks apart, to MPTP-treated, L-DOPA-treated common marmosets primed to exhibit dyskinesia. Prior to GDNF or saline administration, all animals displayed marked dyskinesia when treated with L-DOPA. GDNF administration produced a significant improvement in motor disability and, following the second injection of GDNF, a significant improvement in the locomotor activity was observed. Following the administration of L-DOPA there was a greater reversal of disability and a reduction in the intensity of L-DOPA-induced dyskinesia in GDNF-treated animals compared to saline-treated controls. However, there was no significant difference in L-DOPA's ability to increase locomotor activity between GDNF-treated and saline-treatedanimals. GDNF treatment caused a significant increase in the number of tyrosine hydroxylase-positive neurons in the substantia nigra, but no change in [H-3]mazindol binding to dopamine terminals was found in the striatum of GDNF-treated animals compared to saline-treated controls. In GDNF-treated animals a small but significant reduction in enkephalin mRNA was observed inthe caudate nucleus but not in the putamen or the nucleus accumbens. Substance P mRNA expression was equally reduced in the caudate nucleus and the putamen of the GDNF-treated animals but not in the nucleus accumbens. Intraventricular administration of GDNF improved MPTP-induced disability and reversed dopamine cell loss in the substantia nigra. GDNF also diminished L-DOPA-induced dyskinesia, which may relate to its ability to partly restore nigral dopaminergic transmission or to modify the activity of striatal output pathways.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/01/20 alle ore 14:45:43