Felicitas S. Cabbat

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.

TL;DR: It is reported that MPTP, given to mice at 30 mg/kg intraperitoneally, causes severe and long-lasting depletions of dopamine and its major metabolites dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in the neostriatum.

TL;DR: In vitro oxidation of 1‐Methyl‐4‐phenyl‐ 1,2,5,6 ‐tetrahydropyridine and the fact that MAO‐B inhibitors can protect against MPTP‐induced dopami nergic neurotoxicity in vivo point to an important role for MAO-B in MPTP metabolism in vivo.

TL;DR: 1‐Methyl‐4‐phenyl‐1,2,5,6‐tetrahydropyridine (MPTP) is known to cause a destruction of the dopaminergic nigrostriatal pathway in certain animal species including mice and some structurally related analogs were tested in vitro for their capacity to inhibit the uptake of mouse neostriatal synaptosomal preparations.

TL;DR: Each part of the MPTP molecule is important in determining its neurotoxic activity, and under identical conditions, several MPTP analogues, even those with relatively minor structural changes, were without toxicity.