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

The inter-individual variability of subhuman primates in vulnerability to MPTP is unresolved.

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.

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.

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.

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.