Neuroprotective potential of escitalopram against behavioral, mitochondrial and oxidative dysfunction induced by 3-nitropropionic acid.

backgroundHuntington's disease (HD) is a neurodegenerative syndrome that leads to marked decline in cognitive functioning along with uncharacteristic body movements called chorea. There exists no therapeutic agent to address the disease.3-Nitropropionic acid (3-NP) which is a suicide inhibitor of succinate dehydrogenase and a well-known experimental model to study Huntington's disease, causes substantial impairment in gait and memory through oxidative and neuronal damage. PURPOSE: In the present study protective effect of escitalopram against 3-NP induced neurotoxicity was explored.

methodsAdult female Wistar ratswere subjected to per oral administration of 2 different doses of escitalopram (10 and 20 mg/kg) for 12 days followed by intraperitoneal injection of 3-NP (20 mg/kg) on the last four days.

resultsIntraperitoneal injection of 3-NP lead to significant induction of HD like symptoms in rats such as impaired memory, reduced locomotor activity, hind limb impairment, decreased body weight, oxidative damage and mitochondrial dysfunction. Treatment with 2 different dose of escitalopram helped reverse the mitochondrial enzyme dysfunction along with reversal of behavioural and biochemical anomaly induced by 3-NP. Further, histopathological examination confirmed the neuroprotective potential of escitalopram against 3-NP induced pathological lesions.

conclusionThe results obtained thus substantiate the claim that escitalopram might play an antioxidant and neuroprotective role against 3-NP induced alterations in rats and can prove to be a promising candidate for the management of HD.