Journal ArticleDOI
Monoamine oxidase B(MAO-B) is the major catalyst for 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) oxidation in human brain and other tissues.
TLDR
This assay has been used to show that the rate of oxidation of MPTP parallels that of phenylethylamine in a range of human and rodent tissues, providing strong evidence that this reaction is predominantly catalysed by monoamine oxidase B (MAO-B).About:
This article is published in Neuroscience Letters.The article was published on 1986-02-28. It has received 30 citations till now. The article focuses on the topics: Monoamine oxidase B & MPTP.read more
Citations
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Journal ArticleDOI
Biochemical mechanism of action of the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).
TL;DR: The various biochemical mechanisms considered to explain the selective dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine are reviewed and the implications of the MPTP phenomenon to efforts aimed at elucidating the pathogenesis of idiopathic parkinsonism are discussed.
Journal ArticleDOI
A review of the pharmacology of selegiline.
E. H. Heinonen,R. Lammintausta +1 more
TL;DR: Besides the inhibition of MAO‐B, selegiline also inhibits the uptake of dopamine and noradrenaline into presynaptic nerve and increases the turnover of dopamine, which significantly potentiates the pharmacological effects of levodopa.
Journal ArticleDOI
Pharmacokinetics and metabolism of selegiline
Heinonen E H,Myllylä,Kyösti A. Sotaniemi,Lammintausta R,Salonen J S,Anttila M,Savijärvi M,Kotila M,Rinne U K +8 more
TL;DR: The steady state concentrations of the metabolites in the serum and cerebrospinal fluid of patients with Parkinson's or Alzheimer's diseases who were on continuous selegiline therapy were similar, and were not affected by the addition of levodopa.
Journal ArticleDOI
The neurotoxicity of 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine (mptp) and its relevance to parkinson's disease.
TL;DR: Differences between common laboratory animals and primates which may account for the differences in sensitivity and selectivity of the actions of MPTP are considered as are other factors which may be involved in the neurotoxicity of this compound.
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4-Phenylpyridine (4PP) and MPTP: the relationship between striatal MPP+ concentrations and neurotoxicity.
TL;DR: In vitro studies established that 4PP probably lowers MPP+ concentrations by inhibiting the biotransformation of MPTP to MPP+.
References
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Journal ArticleDOI
Parkinsonism-inducing neurotoxin, N-methyl-4-phenyl-1,2,3,6 -tetrahydropyridine: uptake of the metabolite N-methyl-4-phenylpyridine by dopamine neurons explains selective toxicity.
TL;DR: Blockage of dopamine uptake by mazindol prevents MPTP-induced damage to nigrostriatal dopamine neurons, indicating that MPP+ concentration into dopamine neurons explains their selective destruction by MPTP.
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Dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine in mice
TL;DR: When MPTP (30 milligrams per kilogram of body weight) was administered parenterally to mice, a decrease in concentrations of neostriatal dopamine and its metabolites and a disappearance of nerve cells in the zona compacta of the substantia nigra were observed.
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Protection against the dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine by monoamine oxidase inhibitors.
TL;DR: It is reported that pargyline, nialamide and tranylcypromine, which inhibit both MAO-A andMAO-B, when administered to mice before MPTP, protect against MPTP-induced dopaminergic neurotoxicity.
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Intraneuronal generation of a pyridinium metabolite may cause drug-induced parkinsonism.
TL;DR: It is reported here that MPTP is oxidized in the brain to a pyridinium species (a compound with potent herbicidal activity) and, in the monkey, is trapped intraneuronally and demonstrated that this enzymatic oxidation is blocked in vivo in the mouse by a monoamine oxidase inhibitor, indicating that the oxidative metabolism is required for its neurotoxic effect.
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Immunocytochemical demonstration of monoamine oxidase B in brain astrocytes and serotonergic neurons
TL;DR: The specific distribution of MAO-B in the adult central nervous system indicates that the role of MAB in monoamine metabolism may be more specifically defined than previously believed.