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metadata.artigo.dc.title: Treadmill exercise protects against pentylenetetrazol-induced seizures and oxidative stress after traumatic brain injury
metadata.artigo.dc.creator: Silva, Luiz Fernando Almeida
Hoffmann, Maurício Scopel
Gerbatin, Rogério da Rosa
Fiorin, Fernando da Silva
Dobrachinski, Fernando
Mota, Bibiana Castagna
Wouters, Angelica Terezinha Barth
Pavarini, Saulo Petinatt
Soares, Félix Alexandre Antunes
Fighera, Michele Rechia
Royes, Luiz Fernando Freire
metadata.artigo.dc.subject: EEG
Oxidative stress
Post-traumatic seizure
metadata.artigo.dc.publisher: National Neurotrauma Society 15-Jul-2013
metadata.artigo.dc.identifier.citation: SILVA, L. F. A. et al. Treadmill exercise protects against pentylenetetrazol-induced seizures and oxidative stress after traumatic brain injury. Journal of Neurotrauma, New York, v. 30, n. 14, p. 1278-1287, July 2013.
metadata.artigo.dc.description.abstract: Traumatic brain injury (TBI) is a major cause of acquired epilepsy, and significant resources are required to develop a better understanding of the pathologic mechanism as targets for potential therapies. Thus, we decided to investigate whether physical exercise after fluid percussion injury (FPI) protects from oxidative and neurochemical alterations as well as from behavioral electroencephalographic (EEG) seizures induced by subeffective convulsive doses of pentylenetetrazol (PTZ; 35 mg/kg). Behavioral and EEG recordings revealed that treadmill physical training increased latency to first clonic and tonic-clonic seizures, attenuated the duration of generalized seizures, and protected against the increase of PTZ-induced Racine scale 5 weeks after neuronal injury. EEG recordings also revealed that physical exercise prevented PTZ-induced amplitude increase in TBI animals. Neurochemical analysis showed that exercise training increased glutathione/oxidized glutathione ratio and glutathione levels per se. Exercise training was also effective against alterations in the redox status, herein characterized by lipid peroxidation (thiobarbituric acid reactive substances), protein carbonyl increase, as well as the inhibition of superoxide dismutase and Na+,K+-ATPase activities after FPI. On the other hand, histologic analysis with hematoxylin and eosin revealed that FPI induced moderate neuronal damage in cerebral cortex 4 weeks after injury and that physical exercise did not protect against neuronal injury. These data suggest that the ability of physical exercise to reduce FPI-induced seizures is not related to its protection against neuronal damage; however, the effective protection of selected targets, such as Na+/K+-ATPase elicited by physical exercise, may represent a new line of treatment for post-traumatic seizure susceptibility.
metadata.artigo.dc.language: en_US
Appears in Collections:DMV - Artigos publicados em periódicos

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