1987Canadian Journal of Neurological Sciences / Journal Canadien des Sciences NeurologiquesOpen access

The Use of the MPTP-Treated Mouse as an Animal Model of Parkinsonism

Richard E. Heikkila, Patricia K. Sonsalla

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Abstract

The MPTP-treated mouse has proven to be a valuable model of parkinsonism. For example, C57 black mice treated with MPTP exhibit a large decrement in the neostriatal content of dopamine and its metabolites, a marked reduction in the capacity of neostriatal synaptosomal preparations to accumulate [3H]dopamine, a large decrease in neostriatal tyrosine hydroxylase activity, a marked loss of nerve cells in the zona compacta of the substantia nigra, and pronounced behavioral deficits. These biochemical, pathological and behavioral deficits are similarly observed in MPTP-treated primates and in humans with idiopathic parkinsonism. A great deal of our current knowledge concerning MPTP has come from experimentation carried out in the mouse.

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The MPTP-treated mouse has proven to be a valuable model of parkinsonism. For example, C57 black mice treated with MPTP exhibit a large decrement in the neostriatal content of dopamine and its metabolites, a marked reduction in the capacity of neostriatal synaptosomal preparations to accumulate [3H]dopamine, a large decrease in neostriatal tyrosine hydroxylase activity, a marked loss of nerve cells in the zona compacta of the substantia nigra, and pronounced behavioral deficits. These biochemical, pathological and behavioral deficits are similarly observed in MPTP-treated primates and in humans with idiopathic parkinsonism. A great deal of our current knowledge concerning MPTP has come from experimentation carried out in the mouse.

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Available abstract

The MPTP-treated mouse has proven to be a valuable model of parkinsonism. For example, C57 black mice treated with MPTP exhibit a large decrement in the neostriatal content of dopamine and its metabolites, a marked reduction in the capacity of neostriatal synaptosomal preparations to accumulate [3H]dopamine, a large decrease in neostriatal tyrosine hydroxylase activity, a marked loss of nerve cells in the zona compacta of the substantia nigra, and pronounced behavioral deficits. These biochemical, pathological and behavioral deficits are similarly observed in MPTP-treated primates and in humans with idiopathic parkinsonism. A great deal of our current knowledge concerning MPTP has come from experimentation carried out in the mouse.

Key concepts: MPTP, Parkinsonism, Neuroscience, Animal model, Medicine, Parkinson's disease, Biology, Internal medicine

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