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Please use this identifier to cite or link to this item: http://hdl.handle.net/123456789/2274

Title: Neuroprotective effect of nicotine against 3-nitropropionic acid (3-NP)-induced experimental Huntington’s disease in rats
Authors: Tariq, Mohammad
Khan, Haseeb Ahmad
Elfaki, Ibrahim
Al-Deeb, Saleh
Al-Moutaery, Khalaf
Keywords: Nicotine
Huntington’s Disease
3-Nitropropionic Acid
Issue Date: 2005
Publisher: Elsevier
Citation: Brain Research Bulletin: 67; 161–168
Abstract: Nicotinic acetylcholine receptors (nAChRs) are regarded as potential therapeutic targets to control various neurodegenerative diseases. Owing to the relevance of cholinergic neurotransmission in the pathogenesis of Huntington’s disease (HD) this investigation was aimed to study the effect of nicotine, a nAChR agonist, on 3-nitropropionic acid (3-NP)-induced neurodegeneration in female Wistar rats. Systemic administration of 3-NP in rats serves as an important model of HD. The animals received subcutaneous injections of nicotine (0, 0.25, 0.50 and 1.00 mg/kg) daily for 7 days. 3-NP (25 mg/kg, i.p.) was administered daily 30 min after nicotine for the same duration. One additional group of rats served as control (vehicle only). On day 8, the animals were observed for neurobehavioral performance (motor activity, inclined plane test, grip strength test, paw test and beam balance). Immediately after behavioral studies, the animals were transcardially perfused with neutral buffered formalin (10%) and brains were fixed for histological studies. Lesions in the striatal dopaminergic neurons were assessed by immunohistochemical method using tyrosine hydroxylase (TH) immunostaining. Treatment of rats with nicotine significantly and dosedependently attenuated 3-NP-induced behavioral deficits. Administration of 3-NP alone caused significant depletion of striatal dopamine (DA) and glutathione (GSH), which was significantly and dose-dependently attenuated by nicotine. Preservation of striatal dopaminergic neurons by nicotine was also confirmed by immunohistochemical studies. These results clearly showed neuroprotective effect of nicotine in experimental model of HD. The clinical relevance of these findings in HD patients remains unclear and warrants further studies.
Description: Neuroscience Research Group, Armed Forces Hospital, P.O. Box 7897 (W-912), Riyadh 11159, Saudi Arabia b Department of Biochemistry, College of Science, King Saud University, Riyadh, Saudi Arabia Received 23 April 2005; received in revised form 14 June 2005; accepted 16 June 2005 Available online 26 July 2005
URI: http://hdl.handle.net/123456789/2274
Appears in Collections:College of Science

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