NA+ CURRENTS THAT FAIL TO INACTIVATE

Textbook accounts give the impression that Na+ channels are short-acti ng binary switches: depolarization opens them, but only for about one millisecond. In contrast to this simplified view, a small but signific ant fraction of the total Na+ current in neurons occurs because channe ls open after long delays or in long-duration bursts of openings. Such non-inactivating Na+ current acts physiologically in neurons to ampli fy synaptic potentials and enhance endogenous rhythmicity, and also to aid repetitive firing of action potentials. In glial cells it also ma y regulate Na+-K+ ATPase activity. The evidence for non-inactivating N a+ current in a variety of neurons and glia is reviewed, along with a brief discussion of its own channel substrate and its relevance for ne urological diseases and drug therapy.