Recent studies have determined that K+ channel gene expression is dyna
mically controlled in endocrine, cardiac, and neuronal cells. This reg
ulation is induced by physiological stimuli (e.g., hormones, transmitt
ers, depolarization), drugs (e.g., opiates) and with pathophysiologica
l conditions (e.g,, seizures, hypertension). In many cases, alteration
s in subunit expression are driven by transcriptional changes. Further
more, resultant changes in excitability can be produced within hours b
ecause of the rapid turnover of Kv-channel proteins. Finally, the cons
equences of altering K+-channel subunit are complex because a single g
ene product can participate in forming functionally distinct homomeric
and heteromeric channels in the same cell. Thus, regulating K+-channe
l genes constitutes a novel mechanism for producing intricate long-ter
m changes in excitability. (C) 1998 John Wiley & Sons, Inc.