dc.contributor | Universidade Federal de Sergipe (UFS) | |
dc.contributor | Universidade Federal de São Paulo (UNIFESP) | |
dc.creator | Fighera, M. R. | |
dc.creator | Royes, LFF | |
dc.creator | Furian, A. F. | |
dc.creator | Oliveira, M. S. | |
dc.creator | Fiorenza, N. G. | |
dc.creator | Frussa, R. | |
dc.creator | Petry, J. C. | |
dc.creator | Coelho, R. C. | |
dc.creator | Mello, C. F. | |
dc.date.accessioned | 2016-01-24T12:41:14Z | |
dc.date.accessioned | 2022-10-07T21:33:42Z | |
dc.date.available | 2016-01-24T12:41:14Z | |
dc.date.available | 2022-10-07T21:33:42Z | |
dc.date.created | 2016-01-24T12:41:14Z | |
dc.date.issued | 2006-06-01 | |
dc.identifier | Neurobiology of Disease. San Diego: Academic Press Inc Elsevier Science, v. 22, n. 3, p. 611-623, 2006. | |
dc.identifier | 0969-9961 | |
dc.identifier | http://repositorio.unifesp.br/handle/11600/28952 | |
dc.identifier | 10.1016/j.nbd.2006.01.002 | |
dc.identifier | WOS:000238462600016 | |
dc.identifier.uri | http://repositorioslatinoamericanos.uchile.cl/handle/2250/4030099 | |
dc.description.abstract | Monosialoganglioside (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.language | eng | |
dc.publisher | Elsevier B.V. | |
dc.relation | Neurobiology of Disease | |
dc.rights | http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy | |
dc.rights | Acesso restrito | |
dc.subject | seizure | |
dc.subject | EEG | |
dc.subject | glutaric acid | |
dc.subject | oxidative damage | |
dc.subject | GM1 | |
dc.subject | protein carbonylation | |
dc.subject | TBARS | |
dc.subject | Na+,K+-ATPase activity | |
dc.subject | PTZ | |
dc.title | GMI ganglioside prevents seizures, Na+,K+-ATPase activity inhibition and oxidative stress induced by glutaric acid and pentylenetetrazole | |
dc.type | Artigo | |