Objective: To study on effects and mechanisms of nicotine on dopamine (DA) release in different brain regions of mice model with Parkinson’s disease(PD). Methods: PD mice were established by 1-methyl-4-phenyl-1，2，3，6-tetrahydropyridine (MPTP). Motor function was detected by pole climbing test. The number of dopaminergic neuron in mice midbrain substantia nigra pars compacta(SNpc) region was detected using tyrosine hydroxylase immunohistochemistry. High performance liquid chromatography was used to determine the content of DA in different brain regions (the striatum， hippocampus and cortex). Striatal dopamine transporter (DAT) levels were detected by Western blot. Results: ①Nicotine significantly improved MPTP-induced motor function deficits in wild-type mice; ②Nicotine significantly prevented MPTP-induced dopaminergic neuron loss in wild-type mice SNpc; ③Nicotine significantly inhibited MPTP-induced decrease of striatal DA content in wildtype mice. Nicotine had no significant effect on MPTP-induced decrease of striatal DA content in α7-nicotinic acetylcholine receptors(α7-nAChRs) knockout mice. Nicotine had no obvious effect on DA content in the hippocampus and cortex of MPTP model in wild-type mice or knockout mice. ④Nicotine significantly increased the content of DAT in the striatum of MPTP model in wild-type mice. Nicotine had no effect on MPTP-induced decrease of DAT in the striatum of MPTP model in α7-nAChRs knockout mice. Conclusion: Nicotine inhibits the death of dopaminergic neurons in SNpc region of PD mice and improves striatal DAT levels through the activation of α7-nAChRs. Nicotine promotes the increase of striatal DA content， and exerts neuroprotective effects in PD mice.