ArticleJournal of neural transmission (Vienna, Austria : 1996)2014
6-Hydroxydopamine impairs mitochondrial function in the rat model of Parkinson's disease: respirometric, histological, and behavioral analyses.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- Modulation of Oxidative Stress and Apoptosis by Antrodia cinnamomea-Loaded Citrate-Stabilized Silver Nanoparticles in Experimental Parkinsonism.Molecular neurobiology · 2026Article
- APurinergic signalling · 2026Article
- Investigating Neuroprotective Effects of Berberine on Mitochondrial Dysfunction and Autophagy Impairment in Parkinson's Disease.International journal of molecular sciences · 2025Article
- The specific NQO2 inhibitor, S29434, only marginally improves the survival of dopamine neurons in MPTP-intoxicated mice.Journal of neural transmission (Vienna, Austria : 1996) · 2024Article
- Targeting NAAA counters dopamine neuron loss and symptom progression in mouse models of parkinsonism.Pharmacological research · 2022Article
- Neuroinflammation in Parkinson's Disease - Putative Pathomechanisms and Targets for Disease-Modification.Frontiers in immunology · 2022Review
- Animal models of Parkinson's disease: a guide to selecting the optimal model for your research.Neuronal signaling · 2021Review
- Anti-Apoptotic and Anti-Inflammatory Role of Trans ε-Viniferin in a Neuron-Glia Co-Culture Cellular Model of Parkinson's Disease.Foods (Basel, Switzerland) · 2021Article
- Hesperidin protects against behavioral alterations and loss of dopaminergic neurons in 6-OHDA-lesioned mice: the role of mitochondrial dysfunction and apoptosis.Metabolic brain disease · 2021Article
- Mitochondria as a target for neuroprotection: role of methylene blue and photobiomodulation.Translational neurodegeneration · 2020Review
- Rebamipide Mitigates Impairments in Mitochondrial Function and Bioenergetics with α-Synuclein Pathology in 6-OHDA-Induced Hemiparkinson's Model in Rats.Neurotoxicity research · 2019Article
- Parkinson's disease: experimental models and reality.Acta neuropathologica · 2018Review
- Stress and corticosterone alter synaptic plasticity in a rat model of Parkinson's disease.Neuroscience letters · 2017Article
- Enhanced oxidative capacity of ground squirrel brain mitochondria during hibernation.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Toxin-Induced Experimental Models of Learning and Memory Impairment.International journal of molecular sciences · 2016Review
- Activation of Mitochondrial Complex II-Dependent Respiration Is Beneficial for α-Synucleinopathies.Molecular neurobiology · 2016Article
- Lymphocytes reduce nigrostriatal deficits in the 6-hydroxydopamine mouse model of Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2015Article
- Major Alterations of Phosphatidylcholine and Lysophosphotidylcholine Lipids in the Substantia Nigra Using an Early Stage Model of Parkinson's Disease.International journal of molecular sciences · 2015Article
- Neurotoxin mechanisms and processes relevant to Parkinson's disease: an update.Neurotoxicity research · 2015Article
- Mitochondrial Toxicity by 3-NP Enhanced Susceptibility to Defective Social Behaviors in Male Wistar Rats.Basic and clinical neuroscienceArticle
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Authors and funding
11 authors at 4 institutions in 1 country.
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Abstract
Mitochondrial defects have been shown to be associated with the pathogenesis of Parkinson's disease (PD). Yet, experience in PD research linking mitochondrial dysfunction, e.g., deregulation of oxidative phosphorylation, with neuronal degeneration and behavioral changes is rather limited. Using the 6-hydroxydopamine (6-OHDA) rat model of PD, we have investigated the potential role of mitochondria in dopaminergic neuronal cell death in the substantia nigra pars compacta by high-resolution respirometry. Mitochondrial function was correlated with the time course of disease-related motor behavior asymmetry and dopaminergic neuronal cell loss, respectively. Unilateral 6-OHDA injections (>2.5 μg/2 μl) into the median forebrain bundle induced an impairment of oxidative phosphorylation due to a decrease in complex I activity. This was indicated by increased flux control coefficient. During the period of days 2-21, a progressive decrease in respiratory control ratio of up to -58 % was observed in the lesioned compared to the non-lesioned substantia nigra of the same animals. This decrease was associated with a marked uncoupling of oxidative phosphorylation. Mitochondrial dysfunction, motor behavior asymmetry, and dopaminergic neuronal cell loss correlated with dosage (1.25-5 μg/2 μl). We conclude that high-resolution respirometry may allow the detection of distinct mitochondrial dysfunction as a suitable surrogate marker for the preclinical assessment of potential neuroprotective strategies in the 6-OHDA model of PD.
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