The pyridine derivative 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a potent neurotoxin which selectively destroys nigrostriatal dopamine neurons, producing neurological symptoms relevant to parkinsonism (idiopathic Parkinson’s disease). MPTP exhibits dopaminergic neurotoxicity to humans, monkeys, cats and rodents. The oxidative conversion of MPTP to 1-methyl-4-phenylpyridine (MPP+) is responsible for the generation of its neurotoxicity. This metabolism is mediated by monoamine oxidase B, which in the substantia nigra pars compacta (SNc) is localized specifically in astroglia. Employing various combinations of intra-SNc injections of MPTP and the glutamate analogue gliotoxin L-alpha-aminoadipic acid (L-α-AA), we examined both the dose- and time-dependent effects of selective astroglial ablation on MPTP-induced nigrostriatal neuronal death in the rat. Varying nigrostriatal cell loss was assessed primarily by the aid of fluorescent retrograde axonal tracing. Treatment with MPTP alone caused tremendous nigrostriatal cell loss, while intra-SNc co-injections of MPTP and L-α-AA conferred protection against MPTP neurotoxicity in a dose-dependent fashion. A similar protective action was also exerted by L-α-AA injected just prior to or 1 day before MPTP administration. However, the protective effect of L-α-AA was considerably reduced 3 days after pretreatment. Remarkably, MPTP-induced nigrostriatal cell loss was even enhanced rather than attenuated 7 days following L-α-AA pretreatment. Thus, our data provide clear morphological evidence for the critical importance of the presence of astroglia in the onset of MPTP neurotoxicity.

Astroglial ablation by the glutamate analogue gliotoxin α-aminoadipic acid prevents l-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced nigrostriatal neuronal death

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Astroglial ablation by the glutamate analogue gliotoxin α-aminoadipic acid prevents l-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced nigrostriatal neuronal death