In the mammalian central nervous system (CNS), hypoxia causes a wide range of physiological effects, and these effects often depend on the stage in development. Among the effects are alterations in pH homeostasis. Na⁺-coupled HCO₃- transporters can play critical roles in pH_i regulation and several-such as NCBE and NBCn1-are expressed abundantly in CNS. In the present study we examined the effect of chronic continuous hypoxia on the expression of two electroneutral Na-coupled HCO₃- transporters, SLC4a7 (NBCn1) and SLC4a10 (NCBE) in mouse brain-the first such study on any acid-base transporter. We placed the mice in normobaric chambers and either maintained normoxia (21% inspired O₂) or imposed continuous chronic hypoxia (11% O₂) for a duration of either 14 days or 28 days, starting from ages of either P2 or P90. We assessed protein abundance by western blotting, loading equal amounts of total protein for each condition. In most cases, hypoxia reduced NBCn1 levels by 20-50%, and NCBE levels by 15-40% in cerebral cortex, subcortex, cerebellum and hippocampus-both after 14 and 28 days, and in both pups and adults. We hypothesize that these decreases, which are out of proportion to the expected overall decreases in brain-protein levels, may especially be important for reducing energy consumption.