摘要
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)andγ-aminobutyric acid(GABA)were determined by using the immunocytochem-istry(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 theγ-aminobutyric acid neurons and dopaminergic neurons in the MPTP-treated mice.
基金
supported by the Foundation of Education Department of Liaoning Province,China(No.20060211).