抄録
Secretion of HCO3− at the apical side of the epithelial cells of the choroid plexus is an essential step in the formation of cerebrospinal fluid (CSF). Anion conductance with a high degree of HCO3− permeability has been observed and suggested to be the major pathway for HCO3− transport across the apical membrane, but the molecular entity remains unknown. We identified the first molecular entity of apical choroid plexus HCO3− transport, a novel variant of NBC4 (NBC4g). Electrophysiological studies and pH-recovery assay showed that NBC4g has the electrogenic, DIDS-sensitive, and cAMP-dependent HCO3− transport activity. Furthermore, the contribution of NBC4g to choroid plexus HCO3− transport was demonstrated by RNAi-mediated knockdown of NBC4g using primary cultured cells; treatment with siRNA of NBC4g led to a similar degree of reduction in the transport activity as that observed by treatment with DIDS. Thus, our data strongly indicate that NBC4g is the long-sought transporter responsible for the HCO3− secretion from the choroid plexus into the ventricle thereby controlling the H+ buffering and pH of the CSF. [J Physiol Sci. 2006;56 Suppl:S98]
