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Chloride (Cl−) homeostasis is critical for many cell functions including cell signaling and volume regulation. The action of GABA at GABAA receptors is primarily determined by the concentration of intracellular Cl−. Developmental regulation of intracellular Cl− results in a depolarizing response to GABA in immature neocortical neurons and a hyperpolarizing or shunting response in mature neocortical neurons. One protein that participates in Cl− homeostasis is the neuron-specific K+–Cl− cotransporter (KCC2). Thermodynamic considerations predict that in the physiological ranges of intracellular Cl− and extracellular K+ concentrations, KCC2 can act to either extrude or accumulate Cl−. To test this hypothesis, we examined KCC2 function in pyramidal cells from rat neocortical slices in mature (18–28 d postnatal) and immature (3–6 d postnatal) rats. Intracellular Cl− concentration was estimated from the reversal potential of whole-cell currents evoked by local application of exogenous GABA. Both increasing and decreasing the extracellular K+ concentration resulted in a concomitant change in intracellular Cl−concentration in neurons from mature rats. KCC2 inhibition by furosemide caused a change in the intracellular Cl−concentration that depended on the concentration of pipette Cl−; in recordings with low pipette Cl−, furosemide lowered intracellular Cl−, whereas in recordings with elevated pipette Cl−, furosemide raised intracellular Cl−. In neurons from neonatal rats, manipulation of extracellular K+ had no effect on intracellular Cl− concentration, consistent with the minimal KCC2 mRNA levels observed in neocortical neurons from immature animals. These data demonstrate a physiologically relevant and developmentally regulated role for KCC2 in Cl− homeostasis via both Cl− extrusion and accumulation.

Potassium-Coupled Chloride Cotransport Controls Intracellular Chloride in Rat Neocortical Pyramidal Neurons