Striatal increase of neurotrophic factors as a mechanism of nicotine protection in experimental parkinsonism

R. Maggio, M. Riva, F. Vaglini, F. Fornai, G. Racagni, G. U. Corsini

Research output: Contribution to journalArticle

67 Citations (Scopus)

Abstract

The repeated finding of an apparent protective effect of cigarette smoking on the risk of Parkinson's disease is one of the few consistent results in the epidemiology of this disorder. Among the innumerous substances that originate from tobacco smoke, nicotine is by far the most widely studied, and the most likely candidate for a protective effect against neuronal degeneration in Parkinson's disease. Nicotine is a natural alkaloid that has considerable stimulatory effects on the central nervous system (CNS). Its effects on the CNS are mediated by the activation of neuronal heteromeric acetylcholine-gated ion channel receptors (nAChR, also termed nicotinic acetylcholine receptors). In the present study, we describe the neuroprotective effects of (-)nicotine in two animal models of parkinsonism: the diethyldithiocarbamate (DDC)-induced enhancement of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity in mice, and the methamphetamine-induced neurotoxicity in rats and mice. In parallel experiments, we found that (-)nicotine induces the basic fibroblast growth factor (FGF-2) and the brain-derived neurotrophic factor (BDNF) in rat striatum. As FGF-2 and BDNF have been reported to be neuroprotective for dopaminergic cells, our data indicate that the increase in neurotrophic factors is a possible mechanism by which (-)nicotine protects from experimental parkinsonisms. Moreover, they suggest that nAChR agonists could be of potential benefit in the progression of Parkinson's disease.

Original languageEnglish
Pages (from-to)1113-1123
Number of pages11
JournalJournal of Neural Transmission
Volume104
Issue number10
DOIs
Publication statusPublished - 1997

Fingerprint

Corpus Striatum
Nerve Growth Factors
Parkinsonian Disorders
Nicotine
Fibroblast Growth Factor 2
Parkinson Disease
Brain-Derived Neurotrophic Factor
Nicotinic Receptors
Central Nervous System
Ditiocarb
Cholinergic Agonists
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
Methamphetamine
Neuroprotective Agents
Ion Channels
Alkaloids
Smoke
Acetylcholine
Tobacco
Epidemiology

Keywords

  • Neuroprotection
  • Neurotrophic factor
  • Nicotine
  • Parkinsonism

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Striatal increase of neurotrophic factors as a mechanism of nicotine protection in experimental parkinsonism. / Maggio, R.; Riva, M.; Vaglini, F.; Fornai, F.; Racagni, G.; Corsini, G. U.

In: Journal of Neural Transmission, Vol. 104, No. 10, 1997, p. 1113-1123.

Research output: Contribution to journalArticle

Maggio, R. ; Riva, M. ; Vaglini, F. ; Fornai, F. ; Racagni, G. ; Corsini, G. U. / Striatal increase of neurotrophic factors as a mechanism of nicotine protection in experimental parkinsonism. In: Journal of Neural Transmission. 1997 ; Vol. 104, No. 10. pp. 1113-1123.
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