ArticleNeurochemical research2015
Long-Term Systemic Exposure to Rotenone Induces Central and Peripheral Pathology of Parkinson's Disease in Mice.
Article in Neurochemical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- The Brain-Gut Axis in Parkinson's Disease Pathology.Comprehensive Physiology · 2026Review
- Neuroprotective Effect of Maresin-1 in Rotenone-Induced Parkinson's Disease in Rats: The Putative Role of the JAK/STAT Pathway.Neurochemical research · 2024Article
- Gastrointestinal dysmotility in rodent models of Parkinson's disease.American journal of physiology. Gastrointestinal and liver physiology · 2024Review
- From the Gut to the Brain: The Role of Enteric Glial Cells and Their Involvement in the Pathogenesis of Parkinson's Disease.International journal of molecular sciences · 2024Review
- Effect of Rotenone on the Neurodegeneration among Different Models.Current drug targets · 2024Review
- Phosphorylated SARM1 is involved in the pathological process of rotenone-induced neurodegeneration.Journal of biochemistry · 2023Article
- Synergistic effects of lipopolysaccharide and rotenone on dopamine neuronal damage in rats.CNS neuroscience & therapeutics · 2023Article
- Systemic Rotenone Administration Causes Extra-Nigral Alterations in C57BL/6 Mice.Biomedicines · 2022Article
- Environmental neurotoxic pesticide exposure induces gut inflammation and enteric neuronal degeneration by impairing enteric glial mitochondrial function in pesticide models of Parkinson's disease: Potential relevance to gut-brain axis inflammation in Parkinson's disease pathogenesis.The international journal of biochemistry & cell biology · 2022Article
- Dysregulation of epithelial ion transport and neurochemical changes in the colon of a parkinsonian primate.NPJ Parkinson's disease · 2021Article
- Chronic Systemic Exposure to Low-Dose Rotenone Induced Central and Peripheral Neuropathology and Motor Deficits in Mice: Reproducible Animal Model of Parkinson's Disease.International journal of molecular sciences · 2020Article
- Article
- Oral Exposure to Paraquat Triggers Earlier Expression of Phosphorylated α-Synuclein in the Enteric Nervous System of A53T Mutant Human α-Synuclein Transgenic Mice.Journal of neuropathology and experimental neurology · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a progressive neurodegenerative disease with motor and non-motor symptoms that precede the onset of motor symptoms. Rotenone is often used to induce PD-like pathology in the central nervous system (CNS) and enteric nervous system (ENS). However, there is little or no information on the temporal changes in other neural tissues and the spread of pathology throughout the entire body organs. Here, we recorded the serial immunohistochemical changes in neurons and glial cells of the striatum, substantia nigra (SN), olfactory bulb (OB), thoracic cord (ThC) and ascending colon (AC) induced by 1-, 3- and 6-week administration of rotenone (50 mg/kg/day) infused subcutaneously in C57BL mice using an osmotic pump. Rotenone exposure for 3 or 6 weeks caused neurodegeneration in the striatum, whereas neuronal damage was seen in the SN and OB only after 6 weeks. Moreover, rotenone induced neurodegeneration in the myenteric plexus of AC but not in ThC. Rotenone also activated glial cells before any apparent neurodegeneration in the CNS but not in the ENS. Our results demonstrated that subcutaneous administration of rotenone can cause progressive neurodegeneration in the OB and AC, in addition to the nigrostriatal pathway, and temporal differential glial activation, and that these changes do not spread retrogradely from OB or ENS to nigrostriatal pathway. The results suggested that the different vulnerability of neurons to the neurotoxic effects of rotenone administrated subcutaneously are due to glial activation in these neural tissues.
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