ArticleExperimental neurology2013
Overexpression of parkin in the rat nigrostriatal dopamine system protects against methamphetamine neurotoxicity.
Article in Experimental neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 42 citations in OpenAlex.
- Nrf2 Deficiency Exacerbates Methamphetamine-Induced Neuronal Apoptosis and Cognitive Dysfunction in Male Mice.International journal of molecular sciences · 2026Article
- Neuroinflammatory Mechanisms and Vocalization Biomarkers in theMedical research archives · 2025Article
- Differentially Expressed Nedd4-binding Protein Ndfip1 Protects Neurons Against Methamphetamine-induced Neurotoxicity.Neurotoxicity research · 2025Article
- Interactions of VMAT2 with CDCrel-1 and Parkin in Methamphetamine Neurotoxicity.International journal of molecular sciences · 2024Article
- Methylphenidate and the risk of acute central nervous system oxygen toxicity: a rodent model and observational data in human divers.Diving and hyperbaric medicine · 2024Observational
- Neurotoxic Methamphetamine Doses Alter CDCel-1 Levels and Its Interaction with Vesicular Monoamine Transporter-2 in Rat Striatum.bioRxiv : the preprint server for biology · 2024Article
- Review
- Dopamine and Methamphetamine Differentially Affect Electron Transport Chain Complexes and Parkin in Rat Striatum: New Insight into Methamphetamine Neurotoxicity.International journal of molecular sciences · 2021Article
- Gene Therapeutic Approaches for the Treatment of Mitochondrial Dysfunction in Parkinson's Disease.Genes · 2021Review
- Methamphetamine-induced dopaminergic neurotoxicity as a model of Parkinson's disease.Archives of pharmacal research · 2021Review
- Parkin regulates drug-taking behavior in rat model of methamphetamine use disorder.Translational psychiatry · 2021Article
- PINK1/PARKIN signalling in neurodegeneration and neuroinflammation.Acta neuropathologica communications · 2020Review
- Maackiain Ameliorates 6-Hydroxydopamine andInternational journal of molecular sciences · 2020Article
- Effect of Parkin on methamphetamine-induced α-synuclein degradation dysfunction in vitro and in vivo.Brain and behavior · 2020Article
- Parkin is transcriptionally regulated by the aryl hydrocarbon receptor: Impact on α-synuclein protein levels.Biochemical pharmacology · 2019Article
- Modulation of ARTS and XIAP by Parkin Is Associated with Carnosic Acid Protects SH-SY5Y Cells against 6-Hydroxydopamine-Induced Apoptosis.Molecular neurobiology · 2018Article
- Characterization of Dopaminergic System in the Striatum of Young Adult Park2Scientific reports · 2018Article
- Role of Mitochondria in Methamphetamine-Induced Dopaminergic Neurotoxicity: Involvement in Oxidative Stress, Neuroinflammation, and Pro-apoptosis-A Review.Neurochemical research · 2018Review
- Reduced expression of PARK2 in manganese-exposed smelting workers.Neurotoxicology · 2017Article
- Molecular, Behavioral, and Physiological Consequences of Methamphetamine Neurotoxicity: Implications for Treatment.The Journal of pharmacology and experimental therapeutics · 2017Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Methamphetamine (METH) is a central nervous system psychostimulant with a high potential for abuse. At high doses, METH causes a selective degeneration of dopaminergic terminals in the striatum, sparing other striatal terminals and cell bodies. We previously detected a deficit in parkin after binge METH in rat striatal synaptosomes. Parkin is an ubiquitin-protein E3 ligase capable of protecting dopamine neurons from diverse cellular insults. Whether the deficit in parkin mediates the toxicity of METH and whether parkin can protect from toxicity of the drug is unknown. The present study investigated whether overexpression of parkin attenuates degeneration of striatal dopaminergic terminals exposed to binge METH. Parkin overexpression in rat nigrostriatal dopamine system was achieved by microinjection of adeno-associated viral transfer vector 2/6 encoding rat parkin (AAV2/6-parkin) into the substantia nigra pars compacta. The microinjections of AAV2/6-parkin dose-dependently increased parkin levels in both the substantia nigra pars compacta and striatum. The levels of dopamine synthesizing enzyme, tyrosine hydroxylase, remained at the control levels; therefore, tyrosine hydroxylase immunoreactivity was used as an index of dopaminergic terminal integrity. In METH-exposed rats, the increase in parkin levels attenuated METH-induced decreases in striatal tyrosine hydroxylase immunoreactivity in a dose-dependent manner, indicating that parkin can protect striatal dopaminergic terminals against METH neurotoxicity.
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Registered trials
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