Figure 2.
Effects of TEA on the complex spike are mediated by block of Kv3 channels. Specific blockers of the non-Kv3 TEA-sensitive ion channels were bath applied to determine contributions of these channels to the effects of TEA on the complex spike. IbTx at 100 nm (A), which blocks BK channels, and 100 nm DTX-K (B), which blocks channels containing Kv1.1 subunits, mildly affected the complex spike waveform, typically increasing duration of the complex spike and yielding an additional spikelet (green arrows). C, Linopirdine at 10 μm, blocker of KCNQ channels, had no effect on the complex spike waveform. Unlike the effects of 1 mm TEA, none of these blockers eliminated spikelet expression or considerably affected rate of repolarization of the first spike (right traces). D, DTX-I at 100 nm, which blocks Kv1.1, Kv1.2, and Kv1.6 subunits, did not affect repolarization of the first spike but compromised repetitive spikelet expression and dramatically extended the duration of the complex spike. E, Complex spike recordings from PCs in Kv3.3 KO mice show disrupted spikelet generation and affected repolarization of the first spike. Right traces are overlaid recordings from three Kv3.3 KO and two wild-type PCs at expanded timescales and normalized amplitudes.