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

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.