ArticleMetabolic brain disease2009
MPTP intoxication in mice: a useful model of Leigh syndrome to study mitochondrial diseases in childhood.
Article in Metabolic brain disease, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- LRRK2-mediated mitochondrial dysfunction in Parkinson's disease.The Biochemical journal · 2025Review
- Disease models of Leigh syndrome: From yeast to organoids.Journal of inherited metabolic disease · 2024Review
- Leigh Syndrome: A Tale of Two Genomes.Frontiers in physiology · 2021Review
- Respiratory chain inhibition: one more feature to propose MPTP intoxication as a Leigh syndrome model.Journal of bioenergetics and biomembranes · 2016Article
- The biochemical and cellular basis for nutraceutical strategies to attenuate neurodegeneration in Parkinson's disease.International journal of molecular sciences · 2011Review
- Regional characterization of energy metabolism in the brain of normal and MPTP-intoxicated mice using new markers of glucose and phosphate transport.Journal of biomedical science · 2010Article
- Basal ganglia neuroprotection with anticonvulsants after energy stress: a comparative study.Metabolic brain disease · 2009Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
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Abstract
The basal ganglia, which are interconnected in the striato-nigral dopaminergic network, are affected in several childhood diseases including Leigh syndrome (LS). LS is the most common mitochondrial disorder affecting children and usually arise from inhibition of the respiratory chain. This vulnerability is attributed to a particular susceptibility to energetic stress, with mitochondrial inhibition as a common pathogenic pathway. In this study we developed a LS model for neuroprotection trials in mice by using the complex I inhibitor MPTP. We first verified that MPTP significantly inhibits the mitochondrial complex I in the brain (p = 0.018). This model also reproduced the biochemical and pathological features of LS: MPTP increased plasmatic lactate levels (p = 0.023) and triggered basal ganglia degeneration, as evaluated through dopamine transporter (DAT) autoradiography, tyrosine hydroxylase (TH) immunohistochemistry, and dopamine dosage. Striatal DAT levels were markedly decreased after MPTP treatment (p = 0.003). TH immunoreactivity was reduced in the striatum and substantia nigra (p = 0.005), and striatal dopamine was significantly reduced (p < 0.01). Taken together, these results confirm that acute MPTP intoxication in young mice provides a reproducible pharmacological paradigm of LS, thus opening new avenues for neuroprotection research.
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