Brief Communication

Neurotoxicity Research

, Volume 22, Issue 2, pp 177-180

Protective Effects of Nicotine Against Aminochrome-Induced Toxicity in Substantia Nigra Derived Cells: Implications for Parkinson’s Disease

  • Patricia MuñozAffiliated withDepartment of Molecular & Clinical Pharmacology, Faculty of Medicine, ICBM, University of Chile
  • , Sandro HuenchugualaAffiliated withDepartment of Molecular & Clinical Pharmacology, Faculty of Medicine, ICBM, University of Chile
  • , Irmgard ParisAffiliated withDepartment of Molecular & Clinical Pharmacology, Faculty of Medicine, ICBM, University of Chile
  • , Carlos CuevasAffiliated withDepartment of Molecular & Clinical Pharmacology, Faculty of Medicine, ICBM, University of Chile
  • , Monica VillaAffiliated withDepartment of Molecular & Clinical Pharmacology, Faculty of Medicine, ICBM, University of Chile
  • , Pablo CaviedesAffiliated withDepartment of Molecular & Clinical Pharmacology, Faculty of Medicine, ICBM, University of Chile
  • , Juan Segura-AguilarAffiliated withDepartment of Molecular & Clinical Pharmacology, Faculty of Medicine, ICBM, University of Chile
  • , Yousef TizabiAffiliated withDepartment of Pharmacology, Howard University College of Medicine Email author 

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Abstract

Parkinson’s disease is a debilitating progressive neurodegenerative disorder that results from the loss of or damage to dopaminergic cells containing neuromelanin in the substantia nigra (SN). The underlying neurodegenerative mechanism(s), however, remain elusive. Aminochrome, the precursor of neuromelanin is an endogenous substance capable of inducing selective neurotoxicity to dopaminergic neurons in SN. Nicotine, on the other hand, may offer protective effects against dopaminergic cell damage induced by various neurotoxins including MPTP and salsolinol. In this study, we sought to determine whether nicotine may also protect against aminochrome-induced toxicity in SN derived RCSN-3 cells. Exposure of RCSN-3 cells to a combination of aminochrome (50 μM) and dicoumarol (50 μM) for 48 h induced approximately 70 % cell death. Pretreatment with nicotine, dose-dependently blocked this toxicity. The effects of nicotine in turn were dose-dependently blocked by mecamylamine, a non-selective nicotinic receptor antagonist. These results suggest involvement of nicotinic receptors in protective effects of nicotine against aminochrome-induced toxicity and provide further evidence for possible therapeutic effects of nicotine or nicotinic agonists in Parkinson’s disease.

Keywords

Aminochrome Nicotine RCSN-3 Cells Neurotoxicity Neuroprotection Parkinson’s disease