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Intracellular chloride concentration ([Cl − ] i ) in pancreatic β-cells is kept above electrochemical equilibrium due to the predominant functional presence of Cl −  loaders such as the Na + K + 2Cl −  co-transporter 1 ( Slc12a2 ) over Cl − extruders of unidentified nature. Using molecular cloning, RT-PCR, Western blotting, immunolocalization and  in vitro  functional assays, we establish that the  “neuron-specific”  K + Cl −  co-transporter 2 (KCC2,  Slc12a5 ) is expressed in several endocrine cells of the pancreatic islet, including glucagon secreting α-cells, but particularly in insulin-secreting β-cells, where we provide evidence for its role in the insulin secretory response. Three KCC2 splice variants were identified: the formerly described KCC2a and KCC2b along with a novel one lacking exon 25 (KCC2a-S25). This new variant is undetectable in brain or spinal cord, the only and most abundant known sources of KCC2. Inhibition of KCC2 activity in clonal MIN6 β-cells increases basal and glucose-stimulated insulin secretion and Ca 2+  uptake in the presence of glibenclamide, an inhibitor of the ATP-dependent potassium (K ATP )-channels, thus suggesting a possible mechanism underlying KCC2-dependent insulin release. We propose that the long-time considered  “neuron-specific”  KCC2 co-transporter is expressed in pancreatic islet β-cells where it modulates Ca 2+ -dependent insulin secretion.

The neuronal K+Cl− co-transporter 2 (Slc12a5) modulates insulin secretion