ArticleNeurotoxicity research2018
Striatal Reinnervation Process after Acute Methamphetamine-Induced Dopaminergic Degeneration in Mice.
Article in Neurotoxicity research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Brain dysfunctions and neurotoxicity induced by psychostimulants in experimental models and humans: an overview of recent findings.Neural regeneration research · 2024Article
- 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
- Differential vulnerability of locus coeruleus and dorsal raphe neurons to chronic methamphetamine-induced degeneration.Frontiers in cellular neuroscience · 2022Article
- Evidence for Dopamine Abnormalities Following Acute Methamphetamine Exposure Assessed by Neuromelanin-Sensitive Magnetic Resonance Imaging.Frontiers in aging neuroscience · 2022Article
- Mitochondrial oxidant stress mediates methamphetamine neurotoxicity in substantia nigra dopaminergic neurons.Neurobiology of disease · 2021Article
- Methamphetamine-induced dopaminergic neurotoxicity as a model of Parkinson's disease.Archives of pharmacal research · 2021Review
- Acute MDPV Binge Paradigm on Mice Emotional Behavior and Glial Signature.Pharmaceuticals (Basel, Switzerland) · 2021Article
- The Role of HSP90α in Methamphetamine/Hyperthermia-Induced Necroptosis in Rat Striatal Neurons.Frontiers in pharmacology · 2021Article
- Neuronal and peripheral damages induced by synthetic psychoactive substances: an update of recent findings from human and animal studies.Neural regeneration research · 2020Review
- Early Postnatal Exposure to Paraquat and Maneb in Mice Increases Nigrostriatal Dopaminergic Susceptibility to a Re-challenge with the Same Pesticides at Adulthood: Implications for Parkinson's Disease.Neurotoxicity research · 2020Article
- Catecholaminergic axons in the neocortex of adult mice regrow following brain injury.Experimental neurology · 2020Article
- Pridopidine Induces Functional Neurorestoration Via the Sigma-1 Receptor in a Mouse Model of Parkinson's Disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Article
- Effectiveness of Fragment C Domain of Tetanus Toxin and Pramipexole in an Animal Model of Parkinson's Disease.Neurotoxicity research · 2019Article
- mTOR Modulates Methamphetamine-Induced Toxicity through Cell Clearing Systems.Oxidative medicine and cellular longevity · 2018Article
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Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Methamphetamine (METH), an amphetamine derivate, may increase the risk of developing Parkinson's disease (PD). Human and animal studies have shown that METH produces persistent dopaminergic neurotoxicity in the nigrostriatal pathway, despite initial partial recovery. To determine the processes leading to early compensation, we studied the detailed morphology and distribution of tyrosine hydroxylase immunoreactive fibers (TH-ir) classified by their thickness (types I-IV) before and after METH. Applying three established neurotoxic regimens of METH: single high dose (1 × 30 mg/kg), multiple lower doses (3 × 5 mg/kg) or (3 × 10 mg/kg), we show that METH primarily damages type I fibers (the thinner ones), and to a much lesser extend types II-IV fibers including sterile axons. The striatal TH terminal partial recovery process, consisting of a progressive regrowth increases in types II, III, and IV fibers, demonstrated by co-localization of GAP-43, a sprouting marker, was observed 3 days post-METH treatment. In addition, we demonstrate the presence of growth-cone-like TH-ir structures, indicative of new terminal generation as well as improvement in motor functions after 3 days. A temporal relationship was observed between decreases in TH-expression and increases in silver staining, a marker of degeneration. Striatal regeneration was associated with an increase in astroglia and decrease in microglia expression, suggesting a possible role for the neuroimmune system in regenerative processes. Identification of regenerative compensatory mechanisms in response to neurotoxic agents could point to novel mechanisms in countering the neurotoxicity and/or enhancing the regenerative processes.
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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.