Figure 1.

Acid-base transporters in neuronal excitability regulation in the CNS. At the presynaptic terminal, the activity of acid-extruder NDCBE tends to increase the intracellular [HCO₃ ^-] and pH_i, an effect stimulatory to the spotaneous glutamate release and therefore to the neuronal excitability. At the postsynaptic terminal, the activities of the acid-extruders (such as NHE1, NBCn1, NDCBE, and NBCn2) tend to increase the intracellular [HCO₃ ^-] and pH_i, an effect inhibitory to the activation of KCNQ channels. The inhibition of KCNQ would enhance the neuronal excitability. The activity of acid-loader AE3 would have the opposite effect on the neuronal excitability. The purple shows that, in the absence of extracellular CO₂/HCO₃ ^- in the patch clamp experiments by Jones et al [23], the intracellular CO₂ introduced by the patch pipette would flux out of the cell, a process that would cause akalosis to the pH_i.