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        Increase in the number of striatal neuronal nitric oxide synthase immunoreactive (nNOS-ir) interneurones in MPTP-treated common marmosets primed for and displaying levodopa-induced dyskinesia

        Author
        Peeris, Megawate
        Geraldes, Luiza
        Jackson, Michael
        Hikima, Atsuko
        Broadstock, Martin
        Rose, Sarah
        Jenner, Peter
        Iravani, Mahmoud M.
        Attention
        2299/14432
        Abstract
        In Parkinson’s disease (PD), dyskinesia is a consequence of nigral dopaminergic cell death and chronic levodopa treatment. The cause of levodopa-induced dyskinesia (LID) is unknown but may result from adaptive neuronal changes in the striatum (1). In PD, as well as rodents with an unilateral median forebrain bundle lesion, expression of nNOS mRNA, as well the number of nNOS immunoreactive (-ir) neurones is markedly altered and nNOS inhibitors can reduce levodopa-induced motor abnormalities (2). We counted the number of neuronal nitric oxide synthase immunoreactive (nNOS-ir) interneurones in the caudate nucleus (CN) and putamen (PUT) in normal, drug naïve, common marmosets (n=6) compared to MPTP-treated animals (0.2mg/kg/day, s.c. for 5 consecutive days) that were chronically treated with levodopa (8 mg/kg levodopa plus 10 mg/kg benserazide) but expressed little dyskinesia (n=6) and those that expressed marked dyskinesia (n=7). In the low dyskinesia group (n=6), peak dyskinesia rarely exceeded score 1 and the high dyskinesia group (n=7) scores were >2. The animals were euthanized by pentobarbital sodium (60 mg/kg), and perfuse fixed with 4% paraformaldehyde. Striatal and nigral sections (30 μm) were processed for immunoperoxidase staining for nNOS-ir and tyrosine hydroxylase immunoreactivity (TH-ir) in substantia nigra (SN) and striatum respectively.
        Publication date
        2013
        Published in
        pA2 online
        Other links
        http://hdl.handle.net/2299/14432
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