Na+,K+-ATPase activity impairment after experimental traumatic brain injury: relationship to spatial learning deficits and oxidative stress.
Traumatic brain injury (TBI) is a devastating disease that commonly causes persistent mental disturbances and cognitive deficits. Although studies indicate that oxidative stress and functional deficits occurring after TBI are interrelated events, the knowledge of the mechanisms underlying the development of such cognitive deficits has been limited. Thus, in the present study, we investigated the effect of fluid percussion brain injury (FPI) on a spatial learning task and levels of oxidative stress markers, namely, protein carbonylation and thiobarbituric acid-reactive substances (TBARS) and Na+,K+-ATPase activity 1 or 3 months after FPI in rats. Statistical analysis revealed that FPI increased the scape latency and mean number of error in Barnes maze test 1 and 3 months after FPI. We also found that protein carbonylation and TBARS content increased in the parietal cortex 1 and 3 months after FPI. In addition, 3 months after FPI, protein carbonylation levels increased both in ipsilateral and contralateral cortices of FPI animals. Indeed, statistical analysis revealed a decrease in Na+,K+-ATPase activity in the cerebral cortex of 1 month FPI animals. Furthermore, the decrease in enzyme activity found 3 months was larger, when compared with 1 month after FPI. These results suggest that cognitive impairment following TBI may result, at least in part, from increase of two oxidative stress markers, protein carbonylation and TBARS that occurs concomitantly to a decrease in Na+,K+-ATPase activity.
Centro de Ciências da Saúde, Laboratorio de Psicofarmacologia e Neurotoxicidade, Departamento de Fisiologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil.
Frederico Diniz
FD
Lima
Mauren Assis
MA
Souza
Ana Flávia
AF
Furian
Leonardo Magno
LM
Rambo
Leandro Rodrigo
LR
Ribeiro
Felipe Villa
FV
Martignoni
Maurício Scopel
MS
Hoffmann
Michele Rechia
MR
Fighera
Luiz Fernando Freire
LF
Royes
Mauro Schneider
MS
Oliveira
Carlos Fernando
CF
de Mello
D000818:Animals; D001522:Behavior, Animal / Q000502:physiology*; D001929:Brain Edema / Q000503:physiopathology; D001930:Brain Injuries / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000293:injuries / Q000378:metabolism / Q000503:physiopathology*; D004195:Disease Models, Animal; D007427:Intracranial Pressure / Q000502:physiology; D008297:Male; D018782:Maze Learning / Q000502:physiology; D008568:Memory / Q000502:physiology; D018384:Oxidative Stress; D050050:Protein Carbonylation; D051381:Rats; D017208:Rats, Wistar; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D013037:Spatial Behavior / Q000502:physiology; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D017392:Thiobarbituric Acid Reactive Substances; D000254:Sodium-Potassium-Exchanging ATPase