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Sherer, T.B., Betarbet, R., Testa, C.M., Seo, B.B., Richardson, J.R., Kim, J.H., Miller, G.W., Yagi, T., Matsuno-Yagi, A. and Greenamyre, J.T. (2003) Mechanism of Toxicity in Rotenone Models of Parkinson’s Disease. Journal of Neuroscience, 23, 10756- 10764.
https://doi.org/10.1523/JNEUROSCI.23-34-10756.2003

has been cited by the following article:

• TITLE: Studies on Parkinson’s-Disease-Linked Genes, Brain Urea Levels and Histopathology in Rotenone Induced Parkinson’s Disease Rat Model

  AUTHORS: Suchitra Kavuri, Senthilkumar Sivanesan, Mathew D. Howell, Rajagopalan Vijayaraghavan, Jayakumar Rajadas

  KEYWORDS: Parkinson’s Disease, Rotenone Intraperitoneal and Oral, Brain Urea, Al-pha-Synuclein, Beclin-1, AMP-Activated Protein Kinase, Brain and Liver Pa-thology

  JOURNAL NAME: World Journal of Neuroscience, Vol.10 No.4, November 27, 2020

  ABSTRACT: Parkinson’s disease (PD) is a debilitating neurological disorder that affects the aged population globally. This study aimed to explore how oral- and intraperitoneal-rotenone-induced PD alters brain urea levels, histopathology, and key Parkinsonism-related genes in the striatum. Hematoxylin and eosin staining was performed for histopathology assessment and real-time polymerase chain reaction was performed for gene expression. Rotenone 3 mg/kg body weight (Rot-3-ip) for 21 days and rotenone 50 mg/kg body weight (Rot-50-po) for 28 days significantly (p Snca, Becn1 and Prkaa1 gene expression in the striatum. Lewy bodies were visible in both Rot-3-ip and Rot-50-po rat brains. There were contrasting features in brain and liver histopathology between the oral and intraperitoneal rotenone treatment groups. However, there was no significant (p can have different impacts on the pathological sequence of events based on the molecular approach.