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Increased Na+,K+-ATPase activity in the rat brain after meningitis induction by Streptococcus pneumoniae
Published online by Cambridge University Press: 24 June 2014
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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 by Streptococcus 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 of Streptococcus pneumoniae to 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.
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