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Abstract
Calcium-activated potassium channels are fundamental regulators of neuronal excitability,
participating in interspike interval and spike-frequency adaptation. For large-conductance
calcium-activated potassium (BK) channels, recent experiments have illuminated the
fundamental biophysical mechanisms of gating, demonstrating that BK channels are voltage
gated and calcium modulated. Structurally, BK channels have been shown to possess
an extracellular amino-terminal domain, different from other potassium channels. Domains
and residues involved in calcium-gating, and perhaps calcium binding itself, have
been identified. For small- and intermediate-conductance calcium-activated potassium
channels, SK and IK channels, clones have only recently become available, and they
show that SK channels are a distinct subfamily of potassium channels. The biophysical
properties of SK channels demonstrate that kinetic differences between apamin-sensitive
and apamin-insensitive slow afterhyperpolarizations are not attributable to intrinsic
gating differences between the two subtypes. Interestingly, SK and IK channels may
prove effective drug targets for diseases such as myotonic muscular dystrophy and
sickle cell anemia.