Abstract
Huntington's disease (HD) is a neurodegenerative disease characterized by motor, cognitive and psychological symptoms. Calcium channels play a critical role in the pathophysiology of HD via mediating oxidative and inflammatory damaging mechanisms. 3-nitropropionic acid (3NP) is an inhibitor of succinate dehydrogenase enzyme in the mitochondrial complex II and is used to induce HD like symptoms. This study was designed to investigate the effect of nimodipine, a novel calcium channel blocker on the behavioral and biochemical changes in a 3 NP model of HD in rats. 3-nitropropionic acid (10 mg/kg i.p.) for 14 days significantly reduced locomotor activity in open field in addition to muscle coordination and grip strength in the rotarod test. Furthermore, it impaired memory retention in Morris water maze and triggered a stereotypical behavior in rats. In both striatal and cortical homogenates 3NP reduced superoxide dismutase, non-enzymatic non-protein thiols while increased thiobarbituric acid derivatives and myeloperoxidase activity. Treatment with nimodipine (5mg/kg i.p.) for 14 days; 30 minute prior to 3NP, ameliorated the mentioned deleterious behavioral and biochemical alterations induced by 3NP. The results of this study suggest that calcium channel blockade may have protective effect against HD via modulating oxidative stress and inflammatory pathways.
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