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Effect of chronic oral nicotine on dopaminergic function in the MPTP-treated mouse.

作者信息

Sershen H, Hashim A, Wiener H L, Lajtha A

机构信息

Center for Neurochemistry, Nathan S. Kline Institute for Psychiatric Research, Ward's Island, New York, NY 10035.

出版信息

Neurosci Lett. 1988 Nov 11;93(2-3):270-4. doi: 10.1016/0304-3940(88)90094-8.

DOI:10.1016/0304-3940(88)90094-8
PMID:3266524
Abstract

Although epidemiological studies have suggested a lower incidence of Parkinson's disease in cigarette smokers, repeated exposure to cigarette smoke or nicotine does not protect against neurotoxicity induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Since there is some evidence that nicotinic antagonists, nicotine, and neurotransmitters may have tropic effects on neurite outgrowth, the present study examined the effects of chronic nicotine administration for 16 weeks (in drinking water; 5 mg/kg consumed per day) on the rate of terminal recovery after striatal lesioning with MPTP (2 x 30 mg/kg, s.c.). Terminal recovery, as measured by the rate of recovery in the level of striatal dopamine, was not affected by nicotine. Monoamine oxidase-B activity was not reduced by MPTP, nor did nicotine affect its activity in striatal homogenates.

摘要

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