Nicotine-Induced Neuroprotection in Rotenone In Vivo and In Vitro Models of Parkinson's Disease: Evidences for the Involvement of the Labile Iron Pool Level as the Underlying Mechanism

Neurotoxicity Research
Camila MouhapeGiselle Prunell

Abstract

Parkinson's disease (PD) is characterized by the degeneration of the dopaminergic neurons in the substantia nigra pars compacta (SNpc). Clinical and experimental evidence suggest that the activation of the nicotinic acetylcholine receptor (nAChR) could be protective for PD. In this study, we investigated the neuroprotective capacity of nicotine in a rat PD model. Considering that iron metabolism has been implicated in PD pathophysiology and nicotine has been described to chelate this metal, we also studied the effect of nicotine on the cellular labile iron pool (LIP) levels. Rotenone (1 μg) was unilaterally injected into the median forebrain bundle to induce the degeneration of the nigrostriatal pathway. Nicotine administration (1 mg/K, s.c. daily injection, starting 5 days before rotenone and continuing for 30 days) attenuated the dopaminergic cell loss in the SNpc and the degeneration of the dopaminergic terminals provoked by rotenone, as assessed by immunohistochemistry. Furthermore, nicotine partially prevented the reduction on dopamine levels in the striatum and improved the motor deficits, as determined by HPLC-ED and the forelimb use asymmetry test, respectively. Studies in primary mesencephalic cultures showed that pret...Continue Reading

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Citations

Jun 3, 2020·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Friederike OstendorfLars Tönges
Aug 25, 2020·Journal of Biochemical and Molecular Toxicology·Fatemeh YarmohammadiGholamreza Karimi
Dec 4, 2020·Neural Regeneration Research·Han DengZe-Gang Ma

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Methods Mentioned

BETA
confocal microscopy

Software Mentioned

Ethovision
ImageJ

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