ABSTRACT
In excitable cells in which the intracellular Cl concentration is maintained at a level lower than that at equilibrium, anion channels stabilize the membrane by shifting the membrane potential toward the equilibrium potential for Cl (ECl). In this way, ligand-gated anion channels coupled to GABA or glycine receptors exert an inhibitory effect on neuronal excitation. The resting membrane potential in skeletal muscle is maintained at a very negative level by the activity of a particular type of anion channel, CLC1. To play such an electrogenic role, anion channel operation produces a simple charge separation but does not necessarily result in net Cl transport across the plasma membrane. In nonexcitable epithelial cells, in contrast, anion channels are involved in substantial Cl transport, which eventually results in the absorption or secretion of isotonic NaCl fluids. The bestknown anion channel functioning in a variety of Cl-secreting epithelial cells is the cystic fibrosis transmembrane conductance regulator (CFTR), which is activated by cAMP=PKA.
