Protective effects of nicotine on gamma-aminobutyric acid neurons and dopaminergic neurons in mice with Parkinson disease

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• 作者：Lei Fu (1)
  Yue Li (2)
  Dezheng Gong (1)
  Dengqin Yu (2)
  Jin Gong (3)
  Yanhui Feng (2)
  Yan Peng (1)
  Dongmei Wang (1)
  Hong Xu (1)
  Shengming Yin (2)
  Yiping Sun (1) (2)
  
• 关键词：Parkinson disease ; nicotine ; dopaminergic neuron ; gamma ; aminobutyric acid neuron
• 刊名：Frontiers of Medicine
• 出版年：2009
• 出版时间：September 2009
• 年：2009
• 卷：3
• 期：3
• 页码：330-335
• 全文大小：323KB
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• 作者单位：Lei Fu (1)
  Yue Li (2)
  Dezheng Gong (1)
  Dengqin Yu (2)
  Jin Gong (3)
  Yanhui Feng (2)
  Yan Peng (1)
  Dongmei Wang (1)
  Hong Xu (1)
  Shengming Yin (2)
  Yiping Sun (1) (2)
  
  1. Lab of Physiological Function, College of Basic Medicine, Dalian Medical University, Dalian, 116044, China
  2. Department of Physiology, College of Basic Medicine, Dalian Medical University, Dalian, 116044, China
  3. Department of Anatomy, College of Basic Medicine, Dalian Medical University, Dalian, 116044, China
  

文摘

This study aimed to investigate the protective effect of nicotine on dopaminergic neurons and its mechanisms in mice with Parkinson disease (PD) induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). C57BL/6J mice were injected with MPTP for 8 days to establish a PD model. Nicotine was given for 10 days in the nicotine therapeutic group. Animals were examined behaviorally with the pole test and traction test. Tyrosine hydroxylase (TH) and γ-aminobutyric acid (GABA) were determined by using the immunocytochemistry (ICC) method. The ultrastructural changes of the caudate nucleus (CN) were observed under electron microscopy. The results showed that pretreatment with nicotine could improve the dyskinesia of PD mice markedly. Simultaneously, TH-positive (P<0.01) neurons and GABA-positive (P<0.05) neurons in the nicotine therapeutic group were significantly more than those in the model group. The ultrastructural injury of the nicotine therapeutic group was also ameliorated. Nicotine has protective effects on the γ-aminobutyric acid neurons and dopaminergic neurons in the MPTP-treated mice.