Increased Na+,K+-ATPase activity in the rat brain after meningitis induction by Streptococcus pneumoniae.

Abstract

Barichello T, Generoso JS, Cipriano AL, Casagrande R, Collodel A, Savi GD, Scherer EBS, Kolling J, Wyse ATS. Increase Na+,K+-ATPase activity in the rat brain after meningitis induction byStreptococcus pneumoniae.Background: Pneumococcal meningitis is the most severe infection of the central nervous system with a mortality rate up to 20% and an adverse neurological result in up to 50% of survivors. A complicated series of interactions among the host immune response and oxidants seems to be responsible for meningitis associated brain dysfunctions. Na+,K+-ATPase is an essential enzyme responsible for generating and maintaining the membrane potential necessary for neural excitability, however, the Na+,K+-ATPase activity is altered in several illness;Objective: The aim of this study is to evaluate the Na+,K+-ATPase activity in hippocampus and cortex of the rats submitted to pneumococcal meningitis.Methods: Animals received 10 µl sterile saline as a placebo or an equivalent volume ofStreptococcus pneumoniaeto the concentration of 5 × 109cfu/ml and were killed at 24, 48, 72 and 96 h after meningitis induction. The brain structures, hippocampus and cortex, were immediately isolated on dry ice and stored at −80°C to analyse Na+,K+-ATPase activity.Results: In the hippocampus, we verified the increase of Na+,K+-ATPase activity at 48, 72 and 96 h (p< 0.05) and in the cortex at 24 h (p< 0.05) after pneumococcal meningitis induction.Conclusion: The Na+,K+-ATPase activity is under the control of a diversity of intracellular messengers that are able to modulate the function of the particular isozymes in a precise way. Furthermore, we verified that pneumococcal meningitis increased the Na+,K+-ATPase activity in hippocampus and cortex; this increase can be correlated with a compensatory mechanism in illness pathophysiology.