Highlighted paper selected by editor-in-chief: Parkinsonian rotenone mouse model: reevaluation of long-term administration of rotenone in C57BL/6 mice
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- Inden Masatoshi
- Department of Neurobiology, Kyoto Pharmaceutical University
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- Kitamura Yoshihisa
- Department of Neurobiology, Kyoto Pharmaceutical University
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- Abe Mari
- Department of Neurobiology, Kyoto Pharmaceutical University
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- Tamaki Aya
- Department of Neurobiology, Kyoto Pharmaceutical University
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- Takata Kazuyuki
- Department of Neurobiology, Kyoto Pharmaceutical University
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- Taniguchi Takashi
- Department of Neurobiology, Kyoto Pharmaceutical University
書誌事項
- タイトル別名
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- Parkinsonian Rotenone Mouse Model: Reevaluation of Long-Term Administration of Rotenone in C57BL/6 Mice
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Chronic systemic exposure of Lewis rats to rotenone produced many features of Parkinson's disease (PD), including nigrostriatal dopamine (DA) neurodegeneration and the formation of cytoplasmic inclusions in nigral DA neurons. We also reported that chronic oral administration of rotenone at 30 mg/kg for 28 d caused specific nigrostriatal DA neurodegeneration in C57BL/6 mice. To establish a PD model more suitable for evaluating nigrostriatal DA neurodegeneration, the present study has been designed to assess the neurotoxicity of rotenone after daily oral administration at 30 or 100 mg/kg for 56 d in C57BL/6 mice. The survival rate of rotenone-treated mice at 30 mg/kg did not change from 28 to 56 d, although the survival rate of rotenone-treated mice at 30 mg/kg was decreased to about 70% within one week. The survival rate of the rotenone-treated mice at 100 mg/kg was suddenly decreased after 28 d, and finally to about 15% at 56 d. Rotenone at 30 mg/kg, but not 100 mg/kg, for 28 d caused a significant loss of tyrosine hydroxylase (TH)-positive neurons in the substantia nigra. Rotenone at 100 mg/kg caused a highly variable loss of TH-positive neurons among individual mice. Rotenone at 30 mg/kg for 56 d caused a significant loss of TH-positive neurons and behavioral impairment. In addition, α-synuclein immunoreactivity was increased in surviving TH-positive neurons in a time-dependent manner. Thus, this protocol for chronic administration of rotenone at 30 mg/kg for 56 d is more useful for understanding the mechanism of DA neurodegeneration.
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 34 (1), 92-96, 2011
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390001204626065024
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- NII論文ID
- 130000402269
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- NII書誌ID
- AA10885497
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 10926866
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
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- 抄録ライセンスフラグ
- 使用不可