Effects of Nicotine on MPTP-induced Parkinson's Disease Animal Model.
- Author:
Hyun Joo KIM
1
;
Kyu Hyun PARK
;
Sae Ok OH
;
Yangho KIM
;
Sik YOON
;
Sun Yong BAEK
Author Information
1. Department of Anatomy, Pusan National University School of Medicine, Yangsan 626-770, Korea. sybaek@pusan.ac.kr
- Publication Type:Original Article
- Keywords:
MPTP;
Nicotine;
Dopaminergic neuron;
Parkinson's disease
- MeSH:
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine;
Animals;
Dopamine;
Dopaminergic Neurons;
Models, Animal;
Motor Activity;
Nervous System Diseases;
Nicotine;
Parkinson Disease;
Presynaptic Terminals;
Prevalence;
Specific Gravity;
Substantia Nigra;
Tobacco Products
- From:Korean Journal of Anatomy
2009;42(3):161-169
- CountryRepublic of Korea
- Language:English
-
Abstract:
Parkinson's disease (PD) is a progressive neurological disorder characterized by selective loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Despite extensive researches, the etiology of this disease is still unknown; however, the prevalence of PD is lower in the population of cigarette smokers. In this study, the effects of nicotine were investigated on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson's disease animal model and the spontaneous locomotor activity was analyzed. In comparison with MPTP-induced PD animals, nicotine-treated PD animals exhibited significant improvement in the number of dopaminergic neurons in the SNpc, the relative density of dopaminergic axon terminals in the striatum, and locomotor activity. Also, MPTP-induced astrogliosis was prevented by nicotine treatment. These results suggest that the dopamine depletion in the SNpc and striatum and the decreased spontaneous locomotor activity were prevented by nicotine treatment in the MPTP-induced PD animal model.
