Comparative analysis of dose-dependent neurotoxic response to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in C57BL/6 N mice derived from three different sources

Hwang, Dong-Joo; Kwon, Ki-Chun; Song, Han-Jung; Kim, Kil-Soo; Jung, Young-Suk; Hwang, Dae‐Youn; Cho, Joon-Yong

doi:10.1186/s42826-019-0012-2

Cited by 11 publications

(9 citation statements)

References 21 publications

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“…Hwang et al (2019) administered 10, 20, and 30 mg of MPTP/kg, intraperitoneally four times per day at one-hour intervals in male C57BL/6 N mice. MPTP administration resulted in impairments in motor performances (rotarod and pole test) and the nigrostriatal neurotoxic responses (dopamine, tyrosine hydroxylase positive, and protein carbonylation) [ 149 ]. They observed a similar neurotoxic PD response and locomotor abnormalities impaired dose-dependently [ 149 ].…”

Section: Neurotoxins Used To Induce Pd In Vivo Modelsmentioning

confidence: 99%

“…MPTP administration resulted in impairments in motor performances (rotarod and pole test) and the nigrostriatal neurotoxic responses (dopamine, tyrosine hydroxylase positive, and protein carbonylation) [ 149 ]. They observed a similar neurotoxic PD response and locomotor abnormalities impaired dose-dependently [ 149 ]. Hu et al (2020) administered 15 mg of MPTP/kg, intraperitoneally four times (a cumulative of 60 mg/kg) with or without lipopolysaccharide (5 mg/kg, intraperitoneally) in male C57BL/6 mice models and evaluated the Hua-Feng-Dan and Rannasangpei effects against MPTP neurotoxicity.…”

Section: Neurotoxins Used To Induce Pd In Vivo Modelsmentioning

confidence: 99%

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Behavioral Tests in Neurotoxin-Induced Animal Models of Parkinson’s Disease

Prasad

Hung

2020

Antioxidants

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Currently, neurodegenerative diseases are a major cause of disability around the world. Parkinson’s disease (PD) is the second-leading cause of neurodegenerative disorder after Alzheimer’s disease. In PD, continuous loss of dopaminergic neurons in the substantia nigra causes dopamine depletion in the striatum, promotes the primary motor symptoms of resting tremor, bradykinesia, muscle rigidity, and postural instability. The risk factors of PD comprise environmental toxins, drugs, pesticides, brain microtrauma, focal cerebrovascular injury, aging, and hereditary defects. The pathologic features of PD include impaired protein homeostasis, mitochondrial dysfunction, nitric oxide, and neuroinflammation, but the interaction of these factors contributing to PD is not fully understood. In neurotoxin-induced PD models, neurotoxins, for instance, 6-hydroxydopamine (6-OHDA), 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 1-Methyl-4-phenylpyridinium (MPP+), paraquat, rotenone, and permethrin mainly impair the mitochondrial respiratory chain, activate microglia, and generate reactive oxygen species to induce autooxidation and dopaminergic neuronal apoptosis. Since no current treatment can cure PD, using a suitable PD animal model to evaluate PD motor symptoms’ treatment efficacy and identify therapeutic targets and drugs are still needed. Hence, the present review focuses on the latest scientific developments in different neurotoxin-induced PD animal models with their mechanisms of pathogenesis and evaluation methods of PD motor symptoms.

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Section: Neurotoxins Used To Induce Pd In Vivo Modelsmentioning

confidence: 99%

Section: Neurotoxins Used To Induce Pd In Vivo Modelsmentioning

confidence: 99%

Behavioral Tests in Neurotoxin-Induced Animal Models of Parkinson’s Disease

Prasad

Hung

2020

Antioxidants

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“…C57BL/6NKorl is a novel mouse stock recently developed from the C57BL/6 strain background, the most prevalent strain of inbred mice, by the Korean National Institute of Food and Drug Safety Evaluation (NIFDS) [13,14]. Growing evidence indicates that, with some distinctive features primarily related to body weight (BW), the responses of C57BL/6NKorl mice to various chemicals and physiological stimuli (e.g., MPTP administration, methionine and choline-deficient diet feeding, and fertilization) are similar to other mice of different origins (the United States and Japan) supplied by commercial vendors [14][15][16]. However, there is no evidence base for repeated RST-induced depressive-like phenotypes, especially in C57BL/6NKorl mice.…”

Section: Introductionmentioning

confidence: 99%

Comparative analysis of restraint stress-induced depressive-like phenotypes in C57BL/6N mice derived from three different sources

et al. 2020

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C57BL/6NKorl mice are a novel mouse stock recently developed by the National Institute of Food and Drug Safety Evaluation in Korea. Extensive research into the nature of C57BL/6NKorl mice is being conducted. However, there is no scientific evidence for the phenotypic response to restraint stress (RST), a stress paradigm for modeling depressive disorders, in rodents. In this study, we investigated the repeated RST-induced depressive-like phenotypes in C57BL/6 N mouse substrains (viz., C57BL/6NKorl mice from Korea, C57BL/6NA mice from the United States, and C57BL/6NB mice from Japan) obtained from different sources. The results showed that C57BL/6 N mice derived from various sources exposed to repeated RST resulted in depressive-like phenotypes reflected by a similar degree of behavioral modification and susceptibility to oxidative stress in a duration-dependent manner, except for the distinctive features (increased body weight (BW) and tolerance to the suppression of BW gain by exposure to repeated RST) in C57BL/6NKorl mice. Taken together, the duration-dependent alteration in depressive-like phenotypes by repeated exposure to RST observed in this study may provide valuable insights into the nature of C57BL/6NKorl mice as an alternative animal resource for better understanding of the etiology of depressive disorders and the mechanisms of antidepressant actions.

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“…MPP + readily enters the nigrostriatal neurons via dopamine transporters and induces progressive loss of dopaminergic neurons in the SNpc contributing to striatal dopamine depletion further causing a parkinsonian syndrome [ 19 , 20 ]. Till now, the MPTP-treated PD animal models have been commonly used to unravel various pathological events and explore therapeutic mechanisms due to the similar clinical symptoms in animal to those in patients with PD, reliable and reproducible lesions in the nigrostriatal dopaminergic pathway, and less requirements for experimental technology [ 19 , 21 , 22 ]. In order to create a cellular model that mimicked PD, we exposed the neuroblastoma SH-SY5Y cells to MPP + in this study [ 23 ].…”

Section: Introductionmentioning

confidence: 99%

ADP/ATP translocase 1 protects against an α-synuclein-associated neuronal cell damage in Parkinson’s disease model

Ding

et al. 2021

Cell Biosci

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Background ADP/ATP translocase 1 (ANT1) is involved in the exchange of cytosolic ADP and mitochondrial ATP, and its defection plays an important role in mitochondrial pathogenesis. To reveal an etiological implication of ANT1 for Parkinson’s disease (PD), a neurodegenerative disorder, a mouse model treated with 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine and neuroblastoma cell model induced by 1-methyl-4-pehny1-pyridine were utilized in this study. Results The tissue-specific abundance in ANT1 in mouse brains was accessed using the analysis of Western blot and immunohistochemistry. Down-regulated soluble ANT1 was found to be correlated with PD, and ANT1 was associated with PD pathogenesis via forming protein aggregates with α-synuclein. This finding was confirmed at cellular level using neuroblastoma cell models. ANT1 supplement in neuronal cells revealed the protective roles of ANT1 against cytotoxicity caused by MPP+. Protein interaction assay, coupled with the analysis of LC-MS/MS, silver-stained SDS-PAGE and Western blot against anti-ANT1 antibody respectively, illustrated the interaction of ANT1 with α-synuclein using the expressed α-synuclein as a bite. Additionally, a significant increasing ROSs was detected in the MPP+-treated cells. Conclusions This study indicated that ANT1 was a potentially causative factor of PD, and led to neuropathogenic injury via promoting the formation of protein aggregates with α-synuclein. This investigation potentially promotes an innovative understanding of ANT1 on the etiology of PD and provides valuable information on developing potential drug targets in PD treatment or reliable biomarkers in PD prognostication.

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Comparative analysis of dose-dependent neurotoxic response to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in C57BL/6 N mice derived from three different sources

Cited by 11 publications

References 21 publications

Behavioral Tests in Neurotoxin-Induced Animal Models of Parkinson’s Disease

Behavioral Tests in Neurotoxin-Induced Animal Models of Parkinson’s Disease

Comparative analysis of restraint stress-induced depressive-like phenotypes in C57BL/6N mice derived from three different sources

ADP/ATP translocase 1 protects against an α-synuclein-associated neuronal cell damage in Parkinson’s disease model

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