Effects of ammonia and allopurinol on rat hippocampal NMDA receptors

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dc.authoridDELIBAS, NAMIK/0000-0001-8014-6189
dc.authoridDelibas, Namik/0000-0002-1354-8927
dc.authoridYonden, Zafer/0000-0003-0708-5417
dc.contributor.authorYonden, Zafer
dc.contributor.authorAydin, Mehmet
dc.contributor.authorKilbas, Aynur
dc.contributor.authorDemirin, Hilmi
dc.contributor.authorSutcu, Recep
dc.contributor.authorDelibas, Namik
dc.date.accessioned2024-09-18T19:54:17Z
dc.date.available2024-09-18T19:54:17Z
dc.date.issued2010
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractAmmonia is considered to be the main agent responsible for hepatic encephalopathy which progressively leads to altered mental status. N-methyl-D-aspartate (NMDA) is an ionotropic glutamate receptor, which is involved in synaptogenesis, memory and neurotoxicity. The aim of this study was to investigate the effects of ammonia intoxication and allopurinol, a xanthine oxidase (XO) inhibitor, on NMDA receptor subunits, NR2A and NR2B, in the hippocampus of rats. Thirty-six male rats were divided into three groups (n = 12/group) as follows: (1)control group (phosphate buffered saline (PBS) solution); (2)ammonia group (ammonium acetate, 2.5 mmol/kg), (3)ammonia + allopurinol group (ammonium acetate, 2.5 mmol/kg, allopurinol, 50 mg/kg). Each rat received intraperitoneal injection for 28 days. Western Blotting technique was used for detecting NR2A and NR2B expressions. Both NR2A and NR2B subunit expressions decreased 27 and 11%, respectively, in ammonia group with respect to the control group. Ammonium acetate decreased significantly in NR2A subunit expressions in the hippocampus (p < 0.01). Administration of ammonia + allopurinol caused statistically significant increases in NR2A subunit expressions compared to the ammonia group (p < 0.001). The down-regulation of NMDA receptors caused by ammonium acetate suggest that these receptors may play role in the process of hepatic encephalopathy and using allopurinol may have some protective effects in ammonia toxicity. Copyright (C) 2010 John Wiley & Sons, Ltd.en_US
dc.identifier.doi10.1002/cbf.1636
dc.identifier.endpage163en_US
dc.identifier.issn0263-6484
dc.identifier.issn1099-0844
dc.identifier.issue2en_US
dc.identifier.pmid20084674en_US
dc.identifier.scopus2-s2.0-77249086111en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage159en_US
dc.identifier.urihttps://doi.org/10.1002/cbf.1636
dc.identifier.urihttps://hdl.handle.net/20.500.12483/7622
dc.identifier.volume28en_US
dc.identifier.wosWOS:000275520900009en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofCell Biochemistry and Functionen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectammoniaen_US
dc.subjectallopurinolen_US
dc.subjecthippocampusen_US
dc.subjectneurotoxicityen_US
dc.subjectNMDA receptorsen_US
dc.titleEffects of ammonia and allopurinol on rat hippocampal NMDA receptorsen_US
dc.typeArticleen_US

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