Apr 12, 2014

The 3-NP Model of Striatal Neurodegeneration

Current Protocols in Neuroscience
E Brouillet

Abstract

The mitochondrial toxin 3-nitropropionic acid (3-NP) is an irreversible inhibitor of respiratory chain complex II. Chronic systemic administration of 3-NP to mice, rats, and non-human primates leads to preferential degeneration of the striatum, and produces motor and cognitive symptoms that are highly reminiscent of Huntington's disease (HD). HD is caused by a dominant inherited expansion of CAG repeats in the Huntington gene. Thus, many aspects of HD cannot be mimicked by 3-NP. However, recent research shows that mitochondrial defects and oxidative stress may play a key role in HD pathogenesis, further supporting the potential utility of the 3-NP model of striatal degeneration. First, a basic protocol to produce acute striatal lesions in rats using repeated intraperitoneal injection of 3-NP is described. Second, a more complex protocol that takes advantage of the use of osmotic minipumps to steadily release 3-NP leading to consistent lesions and motor symptoms in Lewis rats is presented.

Mentioned in this Paper

Striatonigral Degeneration, Infantile (Disorder)
Pathogenic Aspects
Huntington gene
Neurobehavioral Manifestations
Abnormal Degeneration
Pathogenesis
Neostriatum
Huntington's Disease Pathway
Toxin
Degenerative Diseases, Spinal Cord

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