In the immature central nervous system (CNS) GABA-mediated excitation is thought to be an important developmental signal. It depends on a high intracellular chloride concentration ([Cl(-)](i)) of the particular neuron. [Cl(-)](i) is a consequence of chloride transport processes across the plasma membrane. The ongoing expression of the KCl-co-transporter KCC2 eventually lowers [Cl(-)](i) in most CNS neurons and thus renders GABA hyperpolarizing. As NCBE, a sodium-dependent chloride-bicarbonate exchanger, also lowers [Cl(-)](i) and may thus modulate the GABA-response, we analyzed its expression during prenatal mouse development before establishment of the mature KCC2 expression. Indeed, NCBE is expressed very early in CNS neurons and precedes the expression of KCC2. Unlike KCC2, NCBE is expressed in the peripheral nervous system and in non-neuronal tissues as the choroid plexus, the dura, and some epithelia including the acid secreting epithelium of the stomach and the duodenal epithelium.
