dc.contributorUniversidade Federal de Sergipe (UFS)
dc.contributorUniversidade Federal de São Paulo (UNIFESP)
dc.creatorFighera, M. R.
dc.creatorRoyes, LFF
dc.creatorFurian, A. F.
dc.creatorOliveira, M. S.
dc.creatorFiorenza, N. G.
dc.creatorFrussa, R.
dc.creatorPetry, J. C.
dc.creatorCoelho, R. C.
dc.creatorMello, C. F.
dc.date.accessioned2016-01-24T12:41:14Z
dc.date.accessioned2022-10-07T21:33:42Z
dc.date.available2016-01-24T12:41:14Z
dc.date.available2022-10-07T21:33:42Z
dc.date.created2016-01-24T12:41:14Z
dc.date.issued2006-06-01
dc.identifierNeurobiology of Disease. San Diego: Academic Press Inc Elsevier Science, v. 22, n. 3, p. 611-623, 2006.
dc.identifier0969-9961
dc.identifierhttp://repositorio.unifesp.br/handle/11600/28952
dc.identifier10.1016/j.nbd.2006.01.002
dc.identifierWOS:000238462600016
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/4030099
dc.description.abstractMonosialoganglioside (GM1) is a glycosphingolipid that protects against some neurological conditions, such as seizures and ischemia. Glutaric acidemia type I (GA-I) is an inherited disease characterized by striatal degeneration, seizures, and accumulation of glutaric acid (GA). in this study, we show that GA inhibits Na+,K+-ATPase activity and increases oxidative damage markers (total protein carbonylation and thiobarbituric acid-reactive substances-TBARS) production in striatal homogenates from rats in vitro and ex vivo. It is also shown that GM1 (50 mg/kg, i.p., twice) protects against GA-induced (4 mu mol/striatum) seizures, protein carbonylation, TBARS increase, and inhibition of Na+,K+-ATI`ase activity ex vivo. Convulsive episodes induced by GA strongly correlated with Na+,K+-ATPase activity inhibition in the injected striatum but not with oxidative stress marker measures. Muscimol (46 pmol/striatum), but not MK-801 (3 nmol/ striatum) and DNQX (8 nmol/striatum) prevented GA-induced convulsions, increase of TBARS and protein carbonylation and inhibition of Na+,K+-ATPase activity. the protection of GM1 and muscimol against GA-induced seizures strongly correlated with Na+,K+-ATPase activity maintenance ex vivo. in addition, GM1 (50-200 mu M) protected against Na+K+-ATPase inhibition induced by GA (6 mM) but not against oxidative damage in vitro. GM1 also decreased pentylenetetrazole (PTZ)-induced (1.8 mu mol/striatum) seizures, Na+,K+-ATPase inhibition, and increase of TBARS and protein carbonyl in the striatum. These data suggest that Na+,K+-ATPase and GABA(A) receptor-mediated mechanisms may play important roles in GA-induced seizures and in their prevention by GM1. (c) 2006 Elsevier Inc. All rights reserved.
dc.languageeng
dc.publisherElsevier B.V.
dc.relationNeurobiology of Disease
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.rightsAcesso restrito
dc.subjectseizure
dc.subjectEEG
dc.subjectglutaric acid
dc.subjectoxidative damage
dc.subjectGM1
dc.subjectprotein carbonylation
dc.subjectTBARS
dc.subjectNa+,K+-ATPase activity
dc.subjectPTZ
dc.titleGMI ganglioside prevents seizures, Na+,K+-ATPase activity inhibition and oxidative stress induced by glutaric acid and pentylenetetrazole
dc.typeArtigo


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