Neuropharmacological approach against MPTP (1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine)-induced mouse model of Parkinson's disease

Acta Neurobiol Exp (Wars). 2011;71(2):269-80. doi: 10.55782/ane-2011-1847.

Abstract

Parkinson's disease (PD) is a common neurodegenerative disease that appears essentially as a sporadic condition. PD is well known to be a chronic and progressive neurodegenerative disease produced by a selective degeneration of dopaminergic neurons in the substantia nigra pars compacta. The main clinical features of PD include tremor, bradykinesia, rigidity and postural instability. Most insights into pathogenesis of PD come from investigations performed in experimental models of PD, especially those produced by neurotoxins. The biochemical and cellular alterations that occur after 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) treatment are remarkably similar to that observed in idiopathic PD. Furthermore, it is well known that acute treatment with MPTP can cause a severe loss of tyrosine hydroxylase and dopamine transporter protein levels and dopamine contents in the striatum of mice, as compared to continuous MPTP treatment. Thus these findings may support the validity of acute MPTP treatment model for unraveling in the neurodegenerative processes in PD. In this review, we discuss the neuroprotective effects of various compounds against neuronal cell loss in an MPTP model of PD. This review may lead to a much better understanding of PD as well as provide novel clues to new targets for therapeutic interventions in PD patients.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antiparkinson Agents / therapeutic use*
  • Corpus Striatum / drug effects
  • Disease Models, Animal
  • Dopamine / metabolism
  • Dose-Response Relationship, Drug
  • Drug Interactions
  • Glial Fibrillary Acidic Protein / metabolism
  • Mice
  • Models, Biological
  • Parkinsonian Disorders / chemically induced*
  • Parkinsonian Disorders / drug therapy*
  • Parkinsonian Disorders / pathology
  • Time Factors
  • Tyrosine 3-Monooxygenase / metabolism

Substances

  • Antiparkinson Agents
  • Glial Fibrillary Acidic Protein
  • Tyrosine 3-Monooxygenase
  • Dopamine