{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T01:51:48Z","timestamp":1791165108238,"version":"4.1.0"},"reference-count":31,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2014,4,10]],"date-time":"2014-04-10T00:00:00Z","timestamp":1397088000000},"content-version":"vor","delay-in-days":9,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["CP Neuroscience"],"published-print":{"date-parts":[[2014,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The mitochondrial toxin 3\u2010nitropropionic acid (3\u2010NP) is an irreversible inhibitor of respiratory chain complex II. Chronic systemic administration of 3\u2010NP to mice, rats, and non\u2010human 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\u2010NP. 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\u2010NP model of striatal degeneration. First, a basic protocol to produce acute striatal lesions in rats using repeated intraperitoneal injection of 3\u2010NP is described. Second, a more complex protocol that takes advantage of the use of osmotic minipumps to steadily release 3\u2010NP leading to consistent lesions and motor symptoms in Lewis rats is presented. <jats:italic>Curr. Protoc. 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