Ncbe is the main basolateral Na+ loading mechanism of the choroid plexus epithelium
Cerebrospinal fluid (CSF) provides a specialized extracellular environment for the central nervous system, which is predominantly produced by the choroid plexus, a highly vascularized epithelial structure whose ion transport processes are fundamental to CSF secretion, composition, and homeostasis. The mechanisms of Na+ entry into choroid plexus epithelial cells (CPECs) from the interstitial side…
The study aimed to determine the primary mechanism responsible for sodium (Na+) loading into choroid plexus epithelial cells (CPECs) as they contribute to cerebrospinal fluid (CSF) secretion, composition, and homeostasis. Researchers utilized fluorescent probes to measure intracellular Na+ levels in CPECs with access to both luminal and basolateral membranes.
Upon removing extracellular Na+, the intracellular Na+ concentration decreased significantly, indicating active Na+ uptake. Recovery of intracellular Na+ to baseline levels depended on the presence of CO2 and HCO3-, a process that was partially inhibited by the NKCC1 inhibitor bumetanide and the TRPv4 inhibitor RN1734. However, inhibition by the HCO3- transport inhibitor DIDS suggested Ncbe's involvement in the Na+ recovery process.
Docking studies revealed that DIDS binding to Ncbe and NBCn1 resembled that of anion exchangers, indicating a covalent-type docking. Inhibition of Ncbe in Ncbe-wt mice compared to Ncbe-ko mice further supported Ncbe as the main Na+ entry mechanism into CPECs. The findings collectively point to Ncbe as the rate-limiting step in vectorial Na+ transport driving CSF secretion.
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