Activation of small conductance calcium-activated potassium (K Ca 2) channels can regulate
neuronal firing and synaptic plasticity. They are characterized by their high sensitivity to the
bee venom toxin apamin, but the mechanism of block is not understood. For example,
apamin binds to both K Ca 2.2 and K Ca 2.3 with the same high affinity (KD∼ 5 pm for both
subtypes) but requires significantly higher concentrations to block functional current (IC 50
values of∼ 100 pm and∼ 5 nm, respectively). This suggests that steps beyond binding are …