ArticleThe Journal of biological chemistry2015
Changes in neuronal dopamine homeostasis following 1-methyl-4-phenylpyridinium (MPP+) exposure.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Estimates of Intracellular Dopamine in Parkinson's Disease: A Systematic Review and Meta-Analysis.Journal of Parkinson's diseasePooled it
- 10d, a Pyridoquinoxaline-Based P-Glycoprotein Inhibitor, Exacerbates MPTP-Induced Neurotoxicity in PC12 Cells.Current issues in molecular biology · 2026Article
- Putamen dopamine synthesis, vesicular storage, and metabolism in Parkinson disease.medRxiv : the preprint server for health sciences · 2026Article
- Modulation of Bromo- and Extra-Terminal Domain (BET) Proteins Exerts Neuroprotective Effects in Cell Culture Models of Parkinson's Disease.Biomedicines · 2026Article
- MPPMolecular biology reports · 2025Article
- Ginkgolide B regulates apoptosis, oxidative stress, and mitochondrial dysfunction in MPPNaunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Evaluating the Role of Lin-11, Isl-1, and Mec-3 Kinases in Dopaminergic Neurodegeneration in a Subacute 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Model of Parkinson's Disease.ACS pharmacology & translational science · 2024Article
- Rethinking Parkinson's disease: could dopamine reduction therapy have clinical utility?Journal of neurology · 2024Review
- Neurotoxicology of dopamine: Victim or assailant?Neurotoxicology · 2024Review
- Initial Molecular Mechanisms of the Pathogenesis of Parkinson's Disease in a Mouse Neurotoxic Model of the Earliest Preclinical Stage of This Disease.International journal of molecular sciences · 2024Article
- Predicting phase-I metabolism of piceatannol: an in silico study.In silico pharmacology · 2024Article
- Alpha synuclein modulates mitochondrial CaNPJ Parkinson's disease · 2023Article
- Mitochondrial Dysfunction and Parkinson's Disease: Pathogenesis and Therapeutic Strategies.Neurochemical research · 2023Review
- Alpha Synuclein Modulates Mitochondrial CabioRxiv : the preprint server for biology · 2023Article
- Patch Amperometry and Intracellular Patch Electrochemistry.Methods in molecular biology (Clifton, N.J.) · 2023Article
- LUHMES Cells: Phenotype Refinement and Development of an MPPInternational journal of molecular sciences · 2023Article
- Circular RNA hsa_circ_0004381 Promotes Neuronal Injury in Parkinson's Disease Cell Model by miR-185-5p/RAC1 Axis.Neurotoxicity research · 2022Article
- Article
- Gene expression in the amygdala and hippocampus of cyclic and acyclic gilts.Journal of animal science · 2022Article
- T cells, α-synuclein and Parkinson disease.Handbook of clinical neurology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
1-Methyl-4-phenylpyridinium (MPP(+)), the active metabolite of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, selectively kills dopaminergic neurons in vivo and in vitro via a variety of toxic mechanisms, including mitochondrial dysfunction, generation of peroxynitrite, induction of apoptosis, and oxidative stress due to disruption of vesicular dopamine (DA) storage. To investigate the effects of acute MPP(+) exposure on neuronal DA homeostasis, we measured stimulation-dependent DA release and non-exocytotic DA efflux from mouse striatal slices and extracellular, intracellular, and cytosolic DA (DAcyt) levels in cultured mouse ventral midbrain neurons. In acute striatal slices, MPP(+) exposure gradually decreased stimulation-dependent DA release, followed by massive DA efflux that was dependent on MPP(+) concentration, temperature, and DA uptake transporter activity. Similarly, in mouse midbrain neuronal cultures, MPP(+) depleted vesicular DA storage accompanied by an elevation of cytosolic and extracellular DA levels. In neuronal cell bodies, increased DAcyt was not due to transmitter leakage from synaptic vesicles but rather to competitive MPP(+)-dependent inhibition of monoamine oxidase activity. Accordingly, monoamine oxidase blockers pargyline and l-deprenyl had no effect on DAcyt levels in MPP(+)-treated cells and produced only a moderate effect on the survival of dopaminergic neurons treated with the toxin. In contrast, depletion of intracellular DA by blocking neurotransmitter synthesis resulted in ∼30% reduction of MPP(+)-mediated toxicity, whereas overexpression of VMAT2 completely rescued dopaminergic neurons. These results demonstrate the utility of comprehensive analysis of DA metabolism using various electrochemical methods and reveal the complexity of the effects of MPP(+) on neuronal DA homeostasis and neurotoxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.