Taurine and MAO B binding sites in the brain of monkeys determine differing responses to MPTP administration.

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.