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Rishabh Singh* and Anant Srivastava


In 1976, MPTP was incidentally discovered by a chemistry student, who was trying to synthesize a synthetic heroin.[1] Others, addicted to heroin, replicated this mistake in the early 1980s and developed severe PD-like symptoms. Dr. Langston recognized the potential of this toxin for creating a valid disease model andsoon identified the effects of MPTP administration in non-human primates and described the impairments that resembled the motor disabilities of idiopathic PD.[2] In 1986, Sonsalla and Heikkila[3] showed that MPTP could have many of the same effects in mice. MPTP is highly lipophilic in nature thus it can easily cross the blood brain barrier, where it binds mainly in astrocyte lysosomes, and there is general agreement that astrocytes convert MPTP to its toxic metabolite, the 1-methyl-4-phenylpyridinium (MPP+) ion.[4,5] Evidence indicates that MPTP enters the glial cells in the striatum or the substantia nigra, where it is cleaved by the monoamine oxidase-B isozyme to form MPP+ (l-methyl-4- phenylpyridinium), the neurotoxic metabolite. MPP+ is known to be anexceptional substrate for the dopamine transporter (DAT), which explains its selectivity for dopaminergic neurons.[6, 7]

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