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Please use this identifier to cite or link to this item: http://hdl.handle.net/123456789/6488

Title: Proglumide, a Cholecystokinin Receptor Antagonist, Exacerbates b , b9 -Iminodipropionitrile-Induced Dyskinetic Syndrome in Rats
Authors: Tariq, Mohammad
Khan, Haseeb Ahmad
Rehana, Zehra
Al-Moutaery, Khalaf
Al-Deeb, Saleh
Keywords: Neurobehavioral Toxicity
Biochemical Studies
Motor Activity
Iminodipropionitrile
Proglumide
Cholecystokinin
Vestibular toxicity
Behavioral syndrome
Neurotoxicity
Oxidative stress
Issue Date: 1998
Publisher: Elsevier Science Inc
Citation: Neurotoxicology and Teratology: 20 (5); 571–579
Series/Report no.: Free radicals
Abstract: Proglumide, a cholecystokinin receptor antagonist, exacerbates b, b9 -iminodipropionitrile-induced dyskinetic syndrome in rats.NEUROTOXICOL TERATOL 20 (5) 571–579, 1998.—The present investigation was undertaken to study the effect of proglumide, a cholecystokinin (CCK) receptor antagonist, on iminodipropionitrile (IDPN)-induced excitation, chorea, and circling (ECC) syndrome in rats.The animals were exposed to IDPN in the dose of 100 mg/kg/day IP for 9 days. Proglumide (PG) was administered IP daily 1 h before IDPN in the doses of 250, 500, and 750 mg/kg body weight in three different groups of rats. The animals were observed daily for neurobehavioral abnormalities including dyskinetic head movements, circling, tail hanging, air righting reflex, locomotor activity, and contact inhibition of the righting reflex. After behavioral studies, blood and brain samples were collected for the analysis of malondialdehyde (MDA), conjugated dienes, vitamin E, and glutathione peroxidase (GSH-Px). The temporal bones were also collected for inner ear histopathology. Our results showed that proglumide significantly and dose-dependently exacerbated the incidence and the severity of IDPN-induced ECC syndrome during the treatment period as well as up to 3 weeks of postdosing. Administration of IDPN produced a significant increase in MDA and conjugated dienes and a decrease in vitamin E and GSH-Px, suggesting the role of oxygen-derived free radicals (ODFR) in IDPN-induced neurotoxicity. Concomitant treatment with proglumide potentiated IDPN-induced oxidative stress. The histopathology of the inner ear showed significantly high degeneration of sensory hair cells in the crista ampullaris of the rats treated with IDPN plus proglumide compared to IDPN-alone-treated animals. Further studies are warranted to determine the role of CCK in nitrile toxicity and drug-induced dyskinesia.
URI: http://hdl.handle.net/123456789/6488
Appears in Collections:College of Medicine

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