Fig. 9.
Both Kv1 and KCNQ channels contributed to the transient firing pattern. A: spiking response of a P11 transient neuron to +160-pA current steps, in control solution (left), solution containing 100 nM α-DTX (middle), and solution containing 100 nM α-DTX + 10 μM linopirdine (right). α-DTX and linopirdine converted the transient response at spike threshold to a sustained-A response. For larger steps, α-DTX by itself increased spike number (see insets in control, α-DTX panels). B: as in A, but for a P15 transient neuron and with 10 μM linopirdine as the solo drug treatment (middle). Linopirdine had no effect at spike threshold, but increased spike number for much larger current steps (inset). Linopirdine blocked ILV at −45 mV by 40% in this neuron (not shown). C: sustained-B neurons also had ILV. At spike threshold in control conditions (+80 pA), the sustained-B firing pattern of a P10 neuron was modestly affected by α-DTX but was converted to the sustained-A pattern by α-DTX + linopirdine. This neuron fired spontaneously in the dual-blocker treatment (right, inset). D–F: LV channel blockers also made transient neurons more like sustained neurons in terms of resting potential (D), current threshold for spiking (E), and input resistance (F).