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Functional Alterations in Striatal Cholinergic and Striato-Nigral Gaba-Ergic Neurons Following 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP) Administration

  • Jun-ichi Taguchi
  • Takuya Kuriyama
  • Kinya Kuriyama
Part of the Advances in Behavioral Biology book series (ABBI, volume 38A)

Abstract

It has been well documented that systemic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP) to humans, monkeys, and mice induces various motor disturbances resembling Parkinson’s disease due to the destruction of nigro-striatal dopaminergic neurons.1–3 Concerning the mechanism of the neurotoxicity, it is considered that the 1-methyl-4-phenylpyridinium ion(MPP+), which is converted from MPTP by monoamine oxidase type B in cerebral glial cells and accumulates in the cell body and/or terminals of the nigro-striatal dopaminergic neuron4,5, induces a significant decrement of dopamine content associated with the inhibition of tyrosine hydroxylase in the striatum,6,7 a significant loss of nerve cells due to the binding to neuromelanin,8,9 and the inhibition of NADH-ubiquinone oxidoreductase10 in the substantia nigra.

Keywords

Tyrosine Hydroxylase Substantia Nigra Dopamine Content Gaba Content MPTP Administration 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1990

Authors and Affiliations

  • Jun-ichi Taguchi
    • 1
  • Takuya Kuriyama
    • 1
  • Kinya Kuriyama
    • 1
  1. 1.Department of PharmacologyKyoto Prefectural University of MedicineKamikyo-ku, Kyoto 602Japan

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