Abstract
K+ channels play key roles in dampening excitability in many types of tissues. In neurons, the large conductance Ca2+-activated K+ (BK) channel inhibits excitability by participating in the fast afterhyperpolarization and limiting neurotransmitter release. Paradoxically, BK currents have also been recently linked to enhancing excitability and seizures. Using a transgenic approach, the dual nature of BK's influence on excitability was investigated. In vivo expression of a gain-of function BK channel alpha subunit (R207Q) recapitulates aspects of both the excitatory and inhibitory influence of BK currents. The direction of influence is dependent upon the relative expression level of wildtype and mutant subunits, the resulting BK current activation kinetics, and interaction with other fast-gated K+ currents.
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