Swimming training prevents pentylenetetrazol-induced inhibition of Na+, K+-ATPase activity, seizures, and oxidative stress.
OBJECTIVE
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.
Souza
Mauren Assis
MA
Departamento de Fisiologia e Farmacologia, Laboratório de Neurotoxicidade e Psicofarmacologia, Centro de Ciências da Saúde, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.
Oliveira
Mauro Schneider
MS
Furian
Ana Flávia
AF
Rambo
Leonardo Magno
LM
Ribeiro
Leandro Rodrigo
LR
Lima
Frederico Diniz
FD
Dalla Corte
Liriana Correa
LC
Silva
Luiz Fernando Almeida
LF
Retamoso
Leandro Thies
LT
Dalla Corte
Cristiane Lenz
CL
Puntel
Gustavo Orione
GO
de Avila
Daiana Silva
DS
Soares
Félix Alexandre Antunes
FA
Fighera
Michele Rechia
MR
de Mello
Carlos Fernando
CF
Royes
Luiz Fernando Freire
LF
D000704:Analysis of Variance; D000818:Animals; D001522:Behavior, Animal; D001835:Body Weight / Q000187:drug effects / Q000502:physiology; D002374:Catalase / Q000378:metabolism; D004195:Disease Models, Animal; D004569:Electroencephalography; D005081:Exercise Therapy / Q000379:methods*; D005452:Fluoresceins; D018698:Glutamic Acid / Q000378:metabolism; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*; D010433:Pentylenetetrazole; D050050:Protein Carbonylation / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D012640:Seizures / Q000139:chemically induced / Q000201:enzymology* / Q000517:prevention & control*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D013223:Statistics as Topic; D013482:Superoxide Dismutase / Q000378:metabolism; D013550:Swimming; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D005452:Fluoresceins; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; D018698:Glutamic Acid; C037631:2',7'-dichlorofluorescein; D002374:Catalase; D013482:Superoxide Dismutase; D000254:Sodium-Potassium-Exchanging ATPase; D010433:Pentylenetetrazole