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dc.contributor.authorIravani, Mahmoud M.
dc.contributor.authorCosta, S.
dc.contributor.authorJackson, M. J.
dc.contributor.authorTel, Banu C.
dc.contributor.authorCannizzaro, C.
dc.contributor.authorPearce, R. K. B.
dc.contributor.authorJenner, P.
dc.date.accessioned2013-06-18T11:00:42Z
dc.date.available2013-06-18T11:00:42Z
dc.date.issued2001-02
dc.identifier.citationIravani , M M , Costa , S , Jackson , M J , Tel , B C , Cannizzaro , C , Pearce , R K B & Jenner , P 2001 , ' GDNF reverses priming for dyskinesia in MPTP-treated, L-DOPA-primed common marmosets ' , European Journal of Neuroscience , vol. 13 , no. 3 , pp. 597-608 .
dc.identifier.issn0953-816X
dc.identifier.otherPURE: 735862
dc.identifier.otherPURE UUID: 3e23f0cc-1a8c-4de6-b613-2465f9f93193
dc.identifier.otherWOS: 000167051800020
dc.identifier.otherScopus: 0035131350
dc.identifier.otherORCID: /0000-0002-4905-9682/work/32997601
dc.identifier.urihttp://hdl.handle.net/2299/10823
dc.description.abstractParkinson's disease (PD) is associated with a progressive loss of dopamine neurons in the substantia nigra and degeneration of dopaminergic terminals in 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 rodent and 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-treated animals. 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 in the 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.en
dc.format.extent12
dc.language.isoeng
dc.relation.ispartofEuropean Journal of Neuroscience
dc.subjectdyskinesia
dc.subjectglial cell line-derived neurotrophic factor
dc.subjectL-DOPA
dc.subjectmarmoset
dc.subjectMPTP
dc.subjectParkinson's disease
dc.subjectLEVODOPA-INDUCED DYSKINESIAS
dc.subjectNIGRAL DOPAMINERGIC-NEURONS
dc.subjectBOLUS INTRAVENTRICULAR-INJECTION
dc.subject6-HYDROXYDOPAMINE IN-VIVO
dc.subjectNEUROTROPHIC FACTOR GDNF
dc.subjectCELL-LINE
dc.subjectPARKINSONS-DISEASE
dc.subjectGENE-EXPRESSION
dc.subjectSUBSTANTIA-NIGRA
dc.subjectGROWTH-FACTOR
dc.titleGDNF reverses priming for dyskinesia in MPTP-treated, L-DOPA-primed common marmosetsen
dc.contributor.institutionDepartment of Human and Environmental Sciences
dc.contributor.institutionSchool of Life and Medical Sciences
dc.contributor.institutionHealth & Human Sciences Research Institute
dc.contributor.institutionPharmacology and Clinical Science Research
dc.contributor.institutionNeurodegenerative Diseases
dc.contributor.institutionAgriculture, Veterinary and Food Sciences
dc.description.statusPeer reviewed
rioxxterms.typeJournal Article/Review
herts.preservation.rarelyaccessedtrue


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