ArticleNeurobiology of disease2021
Mitochondrial oxidant stress mediates methamphetamine neurotoxicity in substantia nigra dopaminergic neurons.
Article in Neurobiology of disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Chronic Methamphetamine Administration Increases Mitochondrial Density and Impairs Mitochondrial Function in the Substantia Nigra Pars Compacta.Journal of neurochemistry · 2026Article
- Decreased Length of Locus Coeruleus Norepinephrine Axons and Increased Amyloid Beta Pathology in Male APP/PS1 Mice During Protracted Abstinence From Alcohol.Neurotoxicity research · 2026Article
- Disruption of Dopamine Homeostasis by Psychostimulants.Molecular neurobiology · 2026Review
- Methamphetamine-Driven Neuroinflammation and Parkinson's Disease Pathology: Mechanistic Insight into Nrf2 and NFĸB Signaling.Molecular neurobiology · 2026Review
- Cubebin Attenuates Methamphetamine-Induced Neurotoxicity Through CREB/BDNF/Caspase-3 Signaling: In Vivo and In Silico Study.Medicina (Kaunas, Lithuania) · 2025Article
- Neurotoxicity mechanisms and clinical implications of six common recreational drugs.Frontiers in pharmacology · 2025Review
- α-Synuclein pathology disrupts mitochondrial function in dopaminergic and cholinergic neurons at-risk in Parkinson's disease.Molecular neurodegeneration · 2024Article
- Review
- Neonatal brain inflammation enhances methamphetamine-induced reinstated behavioral sensitization in adult rats analyzed with explainable machine learning.Neurochemistry international · 2024Article
- Protective effect of melatonin against methamphetamine-induced attention deficits through miR-181/SIRT1 axis in the prefrontal cortex.Molecular biology reports · 2024Article
- Epigenome-wide association study on methamphetamine dependence.Addiction biology · 2024Article
- Microglia: roles and genetic risk in Parkinson's disease.Frontiers in neuroscience · 2024Review
- Isradipine, an L-type calcium channel inhibitor, attenuates cue-associated methamphetamine-seeking in mice.Brain research · 2023Article
- Repeated Methamphetamine Administration Results in Axon Loss Prior to Somatic Loss of Substantia Nigra Pars Compacta and Locus Coeruleus Neurons in Male but Not Female Mice.International journal of molecular sciences · 2023Article
- Long-term methamphetamine self-administration increases mesolimbic mitochondrial oxygen consumption and decreases striatal glutathione.Neuropharmacology · 2023Article
- Deletion ofFrontiers in pharmacology · 2023Article
- Nanowired Delivery of Curcumin Attenuates Methamphetamine Neurotoxicity and Elevates Levels of Dopamine and Brain-Derived Neurotrophic Factor.Advances in neurobiology · 2023Article
- Alterations of Mitochondrial Structure in Methamphetamine Toxicity.International journal of molecular sciences · 2022Article
- Alcohol, neuronal plasticity, and mitochondrial trafficking.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Differential vulnerability of locus coeruleus and dorsal raphe neurons to chronic methamphetamine-induced degeneration.Frontiers in cellular neuroscience · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Methamphetamine abuse is associated with an increased risk of developing Parkinson's disease (PD). Recently, it was found that methamphetamine increases mitochondrial oxidant stress in substantia nigra pars compacta (SNc) dopaminergic neurons by releasing vesicular dopamine (DA) and stimulating mitochondrially-anchored monoamine oxidase (MAO). As mitochondrial oxidant stress is widely thought to be a driver of SNc degeneration in PD, these observations provide a potential explanation for the epidemiological linkage. To test this hypothesis, mice were administered methamphetamine (5 mg/kg) for 28 consecutive days with or without pretreatment with an irreversible MAO inhibitor. Chronic methamphetamine administration resulted in the degeneration of SNc dopaminergic neurons and this insult was blocked by pretreatment with a MAO inhibitor - confirming the linkage between methamphetamine, MAO and SNc degeneration. To determine if shorter bouts of consumption were as damaging, mice were given methamphetamine for two weeks and then studied. Methamphetamine treatment elevated both axonal and somatic mitochondrial oxidant stress in SNc dopaminergic neurons, was associated with a modest but significant increase in firing frequency, and caused degeneration after drug cessation. While axonal stress was sensitive to MAO inhibition, somatic stress was sensitive to Cav1 Ca
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Registered trials
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