Regulation of NBCe1‐A and NBCe1‐B in mouse hippocampal neurons in vitro

Acid‐base transporters are key molecules in the regulation of intracellular pH in many cell types. Among the transporters expressed in neurons, NH 2 ‐terminal variants of the electrogenic sodium‐bicarbonate‐cotransporter 1 A and B (NBCe1‐A and ‐B) are candidates to be involved in intracellular pH regulation since these transporters have been shown to represent key molecules in warranting pH homeostasis in various tissues. In the present study, we have investigated regulation of NBCe1‐A and ‐B under physiological and pathological conditions in vitro using mouse E18.5 primary hippocampal cells. Acute extracellular acidosis resulted in the redistribution of NBCe1‐A from pools in the cell soma towards the processes. After alkali‐load, NBCe1‐B trafficking away from the soma was observed. Transporter redistribution was accompanied by an increase of the plasma membrane fraction. Simulation of normal neuronal activity in vitro resulted in the initiation of NBCe1‐B, but not NBCe1‐A, trafficking along axo‐dendritic structures. The results of the present study indicate that NBCe1‐A and NBCe1‐B trafficking in primary hippocampal neurons is differentially regulated in health and disease.