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Titolo:
Delayed infusion of GDNF promotes recovery of motor function in the partial lesion model of Parkinson's disease
Autore:
Kirik, D; Georgievska, B; Rosenblad, C; Bjorklund, A;
Indirizzi:
Univ Lund, Dept Physiol Sci, Wallenberg Neurosci Ctr, S-22184 Lund, SwedenUniv Lund Lund Sweden S-22184 lenberg Neurosci Ctr, S-22184 Lund, Sweden
Titolo Testata:
EUROPEAN JOURNAL OF NEUROSCIENCE
fascicolo: 8, volume: 13, anno: 2001,
pagine: 1589 - 1599
SICI:
0953-816X(200104)13:8<1589:DIOGPR>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
NIGRAL DOPAMINERGIC-NEURONS; NEUROTROPHIC FACTOR; SUBSTANTIA-NIGRA; IN-VIVO; INTRASTRIATAL 6-HYDROXYDOPAMINE; TYROSINE-HYDROXYLASE; GENE-TRANSFER; TOTAL NUMBER; ADULT-RATS; PROTECTION;
Keywords:
6-hydroxydopamine; cell death; glial cell line-derived neurotrophic factor; Parkinson's disease; paw use; sensorimotor behaviour; stepping; stereology; tyrosine hydroxylase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Kirik, D Univ Lund, Dept Physiol Sci, Wallenberg Neurosci Ctr, BMC A11, S-22184 Lund, Sweden Univ Lund BMC A11 Lund Sweden S-22184 A11, S-22184 Lund, Sweden
Citazione:
D. Kirik et al., "Delayed infusion of GDNF promotes recovery of motor function in the partial lesion model of Parkinson's disease", EUR J NEURO, 13(8), 2001, pp. 1589-1599

Abstract

Here we studied the effects of glial cell line-derived neurotrophic factor(GDNF) in a rat model that represents the symptomatic stages of Parkinson's disease. GDNF was infused starting 2 weeks after an intrastriatal 6-hydroxydopamine (6-OHDA) lesion in order to halt the ongoing degeneration of thenigrostriatal dopaminergic neurons. GDNF or vehicle was infused in the striatum or the lateral ventricle via an osmotic minipump over a total 4-week period (2-6 weeks postlesion). Motor function was evaluated by the stepping, paw reaching and drug-induced motor asymmetry tests before the pump infusion was initiated, and was repeated once during (5 weeks postlesion) and twice after the withdrawal of the minipumps (7 and 11 weeks postlesion). We found that within two weeks following the lesion approximate to 40% of the nigral TH-positive neurons were lost. In the vehicle infusion groups there was an additional 20% cell loss between 2 and 12 weeks after the lesion. This latter cell loss occurred mainly in the caudal part of the SN whereas thecell loss in the rostral SN was almost complete within the first two weeks. Ventricular GDNF infusion completely blocked the late degenerating neurons in the caudal SN and had long lasting behavioural effects on the steppingtest and amphetamine rotation, extending to 6 weeks after withdrawal of the factor. Striatal infusion affected the motor behaviour transiently duringthe infusion period but the motor performance of these animals returned tobaseline upon cessation of the GDNF delivery, and the delayed nigral cell loss was marginally affected. We conclude that intraventricular GDNF can successfully block the already initiated degenerative process in the substantia nigra, and that the effects achieved via the striatal route, when GDNF is given acutely after the lesion, diminish as the fibre terminal degeneration proceeds.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/20 alle ore 16:18:42