Taurine and MAO B binding sites in the brain of monkeys determine differing responses to MPTP administration.
Taurine and MAO B binding sites in the brain of monkeys determine differing responses to MPTP administration.
Where did the research take place?
The study site has not been established. Author addresses may differ from where the research occurred.
Vienna, AT · Author affiliation
Department of Molecular Neurosciences, Center for Brain Research, Medical University of Vienna, Vienna, Austria. Electronic address: christian.pifl@meduniwien.ac.at.Location evidence
Madrid, ES · Author affiliation
Department of Anatomy, Histology and Neuroscience, School of Medicine, Autónoma de Madrid University, Madrid, Spain.Location evidence
Centro, ES · Author affiliation
HM Centro Integral de Neurociencias Abarca Campal (CINAC), Hospital Universitario HM Puerta del Sur, HM Hospitales, Madrid, Spain; Instituto de Investigación Sanitaria, HM Hospitales, Madrid, Spain; Network Center for Biomedical Research on Neurodegenerative Diseases (CIBERNED), Instituto Carlos III, Madrid, Spain; Facultad HM de Ciencias de la Salud de la Universidad Camilo José Cela, Madrid, Spain.Location evidence
Universidad, ES · Author affiliation
HM Centro Integral de Neurociencias Abarca Campal (CINAC), Hospital Universitario HM Puerta del Sur, HM Hospitales, Madrid, Spain; Instituto de Investigación Sanitaria, HM Hospitales, Madrid, Spain; Network Center for Biomedical Research on Neurodegenerative Diseases (CIBERNED), Instituto Carlos III, Madrid, Spain; Facultad HM de Ciencias de la Salud de la Universidad Camilo José Cela, Madrid, Spain.Location evidence
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Original abstract
BACKGROUND: The inter-individual variability of subhuman primates in vulnerability to MPTP is unresolved. NEW METHOD: Therefore, we analysed caudate, putamen, primary motor cortex and prefrontal cortex in groups of monkeys with four distinct stages of MPTP-induced neurodegeneration: (1) staying asymptomatic, (2) recovered from mild parkinsonism, with stable (3) moderate or (4) severe parkinsonism. We determined taurine and the amino acid aspartate by high-pressure gradient system with fluorometric detection, the glial biomarker glial fibrillary acidic protein (GFAP) with quantitative Westernblotting with total protein normalization and MAO B tissue levels with [3H]-L-deprenyl binding and performed correlative analyses. RESULTS: Taurine was higher in asymptomatic and recovered than in control and parkinsonian monkeys, in particular in cortex. [3H]-L-deprenyl binding was higher in putamen and in primary motor cortex of severely parkinsonian monkeys than in asymptomatic and recovered animals. Similarly to [3H]-L-deprenyl, GFAP was increased in putamen of severely parkinsonian monkeys, and a significant correlation of [3H]-L-deprenyl binding with GFAP single values within the four MPTP groups was found. COMPARISON WITH EXISTING METHODS: Instead of comparing different routes of MPTP administration, brain constituents primarily unrelated to the neurodegenerative process were compared in groups of monkeys responding differently to the neurotoxin. CONCLUSIONS: Correlative analyses of the higher taurine levels in asymptomatic and recovered and the higher MAO B levels in severely parkinsonian monkeys in the putamen with, as well as in the cortex without neurodegeneration suggest, that monkeys with less potentially neuroprotective taurine and more MPTP-bioactivating MAO B react more likely with neurodegeneration to MPTP administration.