Figure 11. Percentage block of Ca²⁺-activated Cl⁻ and K⁺ conductances following different treatments suggests the mechanisms of their activation by APs.

Changes in g_Cl,Ca (A) and changes in g_K,Ca1 (B) (measured as total charge transfer) produced by ωCgtx GVIA, ωAga IVA, nifedipine and ryanodine (see also Tables 1 and 2). □, effect after a single AP; , effect following a train. Data were obtained in the presence of 100 nm apamin (A) or 2 mm 9AC (B). Error bars indicate s.e.m. Statistically significant comparisons between different groups are indicated. All changes were significantly different from control (in the absence of any Ca²⁺ current blocker) except those marked * (see Tables 1 and 2). g_Cl,Ca was blocked to a similar extent by all treatments except ωCgtx GVIA. The data suggest that Ca²⁺ from P- and L-type channels must act together to release Ca²⁺ from intracellular stores that, in turn, activates Cl⁻ channels underlying the ADP. In contrast, ωCgtx GVIA markedly reduced g_K,Ca1, suggesting a direct link between Ca²⁺ entering through N-type channels and SK channels underlying the AHP. A small amount of Ca²⁺ entry through L-type channels also contributes to activation of SK channels in type II cells. See text for further discussion.