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Swimming training prevents pentylenetetrazol‐induced inhibition of Na + , K + ‐ATPase activity, seizures, and oxidative stress
Author(s) -
Souza Mauren Assis,
Oliveira Mauro Schneider,
Furian Ana Flávia,
Rambo Leonardo Magno,
Ribeiro Leandro Rodrigo,
Lima Frederico Diniz,
Corte Liriana Correa Dalla,
Silva Luiz Fernando Almeida,
Retamoso Leandro Thies,
Corte Cristiane Lenz Dalla,
Puntel Gustavo Orione,
De Avila Daiana Silva,
Soares Félix Alexandre Antunes,
Fighera Michele Rechia,
De Mello Carlos Fernando,
Royes Luiz Fernando Freire
Publication year - 2009
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2008.01908.x
Subject(s) - tbars , chemistry , oxidative stress , superoxide dismutase , pentylenetetrazol , catalase , reactive oxygen species , glutamate receptor , pharmacology , thiobarbituric acid , biochemistry , lipid peroxidation , medicine , epilepsy , anticonvulsant , receptor , psychiatry
Summary Purpose: In the present study we decided to investigate whether physical exercise protects against the electrographic, oxidative, and neurochemical alterations induced by subthreshold to severe convulsive doses of pentyltetrazole (PTZ). Methods: The effect of swimming training (6 weeks) on convulsive behavior induced by PTZ (30, 45, and 60 mg/kg, i.p.) was measured and different electrographic electroencephalography (EEG) frequencies obtained from freely moving rats. After EEG recordings, reactive oxygen species (ROS) generation, nonprotein sulfhydryl (NPS), protein carbonyl, thiobarbituric acid‐reactive substances (TBARS), superoxide dismutase (SOD), catalase (CAT), Na + , K + ‐ATPase activity, and glutamate uptake were measured in the cerebral cortex of rats. Results: We showed that physical training increased latency and attenuated the duration of generalized seizures induced by administration of PTZ (45 mg/kg). EEG recordings showed that physical exercise decreased the spike amplitude after PTZ administration (all doses). Pearson’s correlation analysis revealed that protection of physical training against PTZ‐induced seizures strongly correlated with NPS content, Na + , K + ‐ATPase activity, and glutamate‐uptake maintenance. Physical training also increased SOD activity, NPS content, attenuated ROS generation per se, and was effective against inhibition of Na + , K + ‐ATPase activity induced by a subthreshold convulsive dose of PTZ (30 mg/kg). In addition, physical training protected against 2′,7′‐dichlorofluorescein diacetate (DCFH‐DA) oxidation, TBARS and protein carbonyl increase, decrease of NPS content, inhibition of SOD and catalase, and inhibition glutamate uptake induced by PTZ. Conclusions: These data suggest that effective protection of selected targets for free radical damage, such as Na + , K + ‐ATPase, elicited by physical training protects against the increase of neuronal excitability and oxidative damage induced by PTZ.