Fig. 8.

BK proexcitatory effects are mediated by RyR BK channel coupling that increases the fAHP. A: fast-gated BK potassium channels (lacking β₄, blue) are activated during the repolarization phase by calcium influx originating from L-type voltage-dependent calcium channels (orange). Different voltage-dependent calcium channels (including T type, red) specifically contribute to calcium-induced calcium release through RyRs (orange) to activate BK channels and increase the fAHP amplitude. B: fAHP, mediated by RyR-BK channel coupling, causes a shorter ISI to confer the BK channel's proexcitatory effect (red trace). Block of BK channels, block of RyRs, or slow-gating conferred by β₄ reduces the fAHP amplitude and increases the ISI (blue trace).