@article{ref1,
title="Neuroprotective potential of escitalopram against behavioral, mitochondrial and oxidative dysfunction induced by 3-nitropropionic acid",
journal="Annals of neurosciences",
year="2015",
author="Shetty, S. and Hariharan, A. and Shirole, T. and Jagtap, A.G.",
volume="22",
number="1",
pages="11-18",
abstract="BACKGROUND: Huntington'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. <br><br>PURPOSE: In the present study protective effect of escitalopram against 3-NP induced neurotoxicity was explored. <br><br>METHODS: Adult 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. <br><br>RESULTS: Intraperitoneal 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. <br><br>CONCLUSION: The 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. © 2015, Indian Academy of Neurosciences. All rights reserved.<p /><p>Language: en</p>",
language="en",
issn="0972-7531",
doi="10.5214/ans.0972.7531.220104",
url="http://dx.doi.org/10.5214/ans.0972.7531.220104"
}