NDLI: Counteraction by Nitric Oxide Synthase Inhibitor of Neurochemical Alterations of Dopaminergic System in 6-OHDA-Lesioned Rats Under l-DOPA Treatment

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Counteraction by Nitric Oxide Synthase Inhibitor of Neurochemical Alterations of Dopaminergic System in 6-OHDA-Lesioned Rats Under l-DOPA Treatment

Content Provider	Springer Nature Link
Author	Del Bel, Elaine Padovan Neto, Fernando Eduardo Szawka, Raphael Escorsim da Silva, Célia Aparecida Raisman Vozari, Rita Anselmo Franci, Janete RomaDutra, Angélica Caroline Guimaraes, Francisco Silveira
Copyright Year	2013
Abstract	Nitric oxide synthase inhibitors reduce l-3, (Del-Bel et al., Cell Mol Neurobiol 25(2):371–392, 2005) 4-dihydroxyphenylalanine (l-DOPA)-induced abnormal motor effects subsequent to depletion of dopaminergic neurons in rodents and non-human primates. The present study used quantitative high-performance liquid chromatography to analyze, for the first time, dopamine metabolism in striatum of rats in order to elucidate the mechanism of action of the nitric oxide synthase inhibitors. Adult male Wistar rats received unilateral microinjection of saline (sham) or 6-hydroxydopamine (6-OHDA-lesioned) in the medial forebrain bundle. Past 3 weeks, rats were treated during 21 days with l-DOPA/benserazide (30 mg/kg/7.5 mg/kg, respectively, daily). On the 22nd day rats received an intraperitoneal (i.p.) injection of either vehicle or 7-nitroindazole, a preferential neuronal nitric oxide synthase inhibitor before l-DOPA. Abnormal involuntary movements and rotarod test were assessed as behavioral correlate of motor responses. Lesion intensity was evaluated through tyrosine hydroxylase immunohystochemical reaction. Dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), and an extent of dopamine striatal tissue levels/dopamine metabolism were measured in the striatum. Lesion with 6-OHDA decreased dopamine, DOPAC, and DOPAC/dopamine ratio in the lesioned striatum. l-DOPA treatment induced abnormal involuntary movements and increased DOPAC/dopamine ratio (nearly five times) in the lesioned striatum. l-DOPA-induced dyskinesia was mitigated by 7-nitroindazole, which also decreased dopamine turnover, dopamine and DOPAC levels. Our results revealed an almost two times increase in dopamine content in the non-lesioned striatum of 6-OHDA-lesioned rats. Reduction of striatal DOPAC/dopamine ratio in dyskinetic rats may suggest an increase in the dopamine availability. Our data confirm contribution of nitrergic transmission in the pathogenesis of l-DOPA-induced dyskinesia with potential utilization of nitric oxide synthase inhibitors for treatment.
Starting Page	33
Ending Page	44
Page Count	12
File Format	PDF
ISSN	10298428
Journal	Neurotoxicity Research
Volume Number	25
Issue Number	1
e-ISSN	14763524
Language	English
Publisher	Springer US
Publisher Date	2013-06-27
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Dopamine turnover Parkinson’s disease l-DOPA-induced dyskinesia Dopamine replacement therapy Motor complications Neurosciences Neurology Neurochemistry Pharmacology/Toxicology Neurobiology Cell Biology
Content Type	Text
Resource Type	Article
Subject	Neuroscience Toxicology

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