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Assessment of Sensorimotor Function in Mouse Models of Parkinson's Disease
Published on: June 17, 2013
S100B transgenic mice develop features of Parkinson's disease
Jialin Liu1, Hailin Wang, Lianfeng Zhang
1Institute of Laboratory Animal Sciences, Chinese Academy of Medical Sciences & Comparative Medical Center, Peking Union Medical College, Panjiayuan No. 5, Chaoyang, Beijing, P.R. China.
Archives of Medical Research
|March 8, 2011
Summary
Overexpressing the S100B gene in mice impaired motor coordination, potentially due to altered dopamine and serotonin levels. This suggests S100B may play a role in Parkinson's disease pathogenesis.
Area of Science:
- Neuroscience
- Genetics
- Molecular Biology
Background:
- Parkinson's disease (PD) is a common neurodegenerative disorder with unknown causes.
- Further research is needed to understand PD mechanisms.
- This study investigates the role of S100B in PD development.
Purpose of the Study:
- To create brain-specific S100B gene transgenic mice.
- To investigate the role of S100B in the development of Parkinson's disease.
Main Methods:
- Constructed a human S100B gene transgenic vector using the PDGF promoter.
- Produced transgenic mice via microinjection.
- Assessed motor coordination using the Rota-rod test.
- Measured gene and protein expression (D1DR, D2DR, GRK2, GRK5, TH) and neurotransmitter levels (DOPA, DA, HVA, 5-HT, 5-HIAA) using RT-PCR, Western blotting, and HPLC-FLD.
Main Results:
- Transgenic mice (TG) showed impaired motor coordination compared to controls (CG).
- TG mice exhibited decreased D2DR and GRK2 expression and reduced 5-HT levels.
- TG mice displayed increased DOPA, DA, and HVA levels.
- S100B knockout mice (KG) showed no significant changes compared to CG.
Conclusions:
- Brain S100B overexpression leads to motor coordination deficits.
- These deficits may stem from D2DR and GRK2 downregulation, altered dopamine metabolism, and decreased serotonin.
- S100B is implicated as a potential factor in Parkinson's disease pathogenesis.
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