We investigated the effect of high (12, 20, and 50 mM) extracellular K+ concentrations ([K+]0) on [U-14C] acetate oxidation to CO2 in cerebral cortex slices of control and perinatal malnourished rats. High [K+]o increased the acetate oxidation, compared with a medium containing 2.7 mM [K+]0. By investigating the mechanisms involved in this stimulation, it was shown that (i) ouabain (1 mM) and monensin (10 microM) prevented this increase; (ii) in a medium with physiological [K+]0 (2.7 mM), the decreasing of [Na+]0 stimulated acetate oxidation. These results suggest that the stimulatory effect of [K+]0 on acetate oxidation was due to the decreasing of Na1 levels. Considering that malnutrition could alter the activity of Na+,K(+)-ATPase and/or other pertinent proteins, its effect on acetate oxidation was investigated. The malnutrition, which altered the body and cerebral weight of rats, did not modify the acetate oxidation in any protocol.