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2009, Volume 3, Issue 3

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Frontiers of Medicine >> 2009, Volume 3, Issue 3 doi: 10.1007/s11684-009-0051-4

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

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; 4.Lab of Physiological Function, College of Basic Medicine, Dalian Medical University, Dalian 116044, China；Department of Physiology, College of Basic Medicine, Dalian Medical University, Dalian 116044, China;

Available online: 2009-09-05
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Abstract

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 ( < 0.01) neurons and GABA-positive ( < 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.

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