Details

Autor(en) / Beteiligte

• 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

Titel

Swimming training prevents pentylenetetrazol‐induced inhibition of Na+, K+‐ATPase activity, seizures, and oxidative stress

Ist Teil von

• Epilepsia (Copenhagen), 2009-04, Vol.50 (4), p.811-823

Ort / Verlag

Oxford, UK: Blackwell Publishing Ltd

Erscheinungsjahr

2009

Quelle

Free E-Journal (出版社公開部分のみ）

Beschreibungen/Notizen

• 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.