Time course of MPTP-induced degeneration of the nigrostriatal dopamine system in C57 BL/6 mice
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Cited by (37)
The integrated stress response as a key pathway downstream of mitochondrial dysfunction
2022, Current Opinion in PhysiologyCitation Excerpt :Mitochondrial dysfunction is the cornerstone of neurodegenerative diseases. The initial link between mitochondrial dysfunction and neurodegeneration was suggested with the discovery of neurotoxins that inhibit complex I, such as MPTP and rotenone, causing irreversible damages in the nigrostriatal brain region [105]. Consistent with this, deletion of Ndufs2, a component of the catalytic core of complex I, causes dopaminergic neuron loss in the substantia nigra and the striatum along with motor disabilities in mice [106].
Dynamic changes of activated AHR in microglia and astrocytes in the substantia nigra-striatum system in an MPTP-induced Parkinson's disease mouse model
2021, Brain Research BulletinCitation Excerpt :Firstly, we induced the PD model by intraperitoneal injection of the neurotoxin MPTP. As expected, TH immunoreactivity was gradually decreased in the striatum and the SNpc at each time point after MPTP treatment, with the maximal decrease observed at day 8, coinciding with the pattern of dopamine concentration changes (Sundström et al., 1988). In the meantime, we found that the expression of MAO-B was higher in PD groups, especially at the time point of day 6 after MPTP treatment, indicating that the maximal DA reduction may occur at this time point in our model (Hare et al., 2013; Dauer and Przedborski, 2003).
Aberrant Tonic Inhibition of Dopaminergic Neuronal Activity Causes Motor Symptoms in Animal Models of Parkinson's Disease
2020, Current BiologyCitation Excerpt :Therefore, the protective effect of genetic deletion or pharmacological inhibition of MAO-B in PD models could be attributed to any one of these possible actions of MAO-B. To bypass the MAO-B’s action of MPP+ conversion, we always treated the animals with selegiline 3 days after MPTP treatment. During the 3 days, all of the MPTP should have been converted to MPP+ [55], and any alleviating effect by selegiline should be independent of MAO-B’s action of MPP+ conversion. The other possibility that the protective effect in MAO-B KO mice is due to the lack of dopamine degradation is unlikely because MAO-B KO mouse is reported to display an unaltered striatal dopamine level [56].
Medicinal plant Combretum leprosum mart ameliorates motor, biochemical and molecular alterations in a Parkinson's disease model induced by MPTP
2016, Journal of EthnopharmacologyCitation Excerpt :Following systemic administration, MPTP is metabolised by monoamine oxidase B (MAO-B) in the glial cells, resulting in the metabolite 1-methyl-4-phenylpyridine (MPP+), which exhibits high affinity for the SNpc dopaminergic neurons. Once inside the neurons, MPP+ accumulates within the mitochondria, causing the inhibition of the electron transport chain complex I and, consequently, neuronal cell death by apoptosis, resulting in striatal DA depletion (Sundstrom et al., 1988). The analysis of the striatal dopamine metabolism in the treatment regimen used in the present work, demonstrated that MPTP was able to induce a significant reduction of dopamine and its metabolites DOPAC and HVA.
Genetic and pharmacological evidence that endogenous nociceptin/orphanin FQ contributes to dopamine cell loss in Parkinson's disease
2016, Neurobiology of DiseaseCitation Excerpt :Nonetheless, the contribution of the different neurotoxicity mechanisms/pathways varies depending on the protocol of MPTP administration. Indeed, in the acute MPTP model, DA neurons die rapidly, within 4 days from toxin administration (Jackson-Lewis and Przedborski, 2007; Sundstrom et al., 1988), through non-apoptotic (Jackson-Lewis and Przedborski, 2007), perhaps microglia-mediated inflammatory (Furuya et al., 2004; Liberatore et al., 1999) mechanisms. Conversely, in the subacute MPTP model, neuronal death is delayed, and apoptosis along with astrocyte activation is clearly observed (Serra et al., 2002; Tatton and Kish, 1997).