Background & Objective: The large conductance, calcium- and voltage-activated potassium
channels (BK) are widely distributed channel proteins which exist in virtually every cell type of
mammals and function to influence membrane excitability and Ca2+ signaling. BK channels can be activated
by the increase of the intracellular Ca2+ concentration, a consequence of neuronal excitation,
and then terminate the action potential with the outward K+ flux. Moreover, after-hyperpolarization
induced by BK channels closes Cav channels and thus precludes excessive Ca2+ influx. Considering
this negative feedback effect, BK channel seemly acts to decrease membrane excitability in order to
prevent hyperexcitation which is a typical characteristic of epilepsy. Therefore, one may reasonably
suppose that membrane excitability would increase when the BK channel activity decreases. However,
the membrane excitability displays elevation when the function of BK channel is under either upregulated
or down-regulated status. Factors altering the activity of BK channels, such as gene mutations,
polymorphism, channel openers or blockers that lead to loss- or gain-of-function, have all been
linked to epilepsy onset.
Conclusion: The aim of this review is to summarize existing knowledge and recent findings on the
molecular properties, signaling complex and channel dysfunction of the BK channels with a particular
attention to the possible relevance to the pathophysiology of epilepsy.