Ih regulates rebound spike latency. (A) Representative traces of rebound spikes recorded from a WT SGN (P3, base) in three different conditions, control, 100 µM nickel, and both nickel and 100 µM ZD7288. Note that calcium channel blocker, nickel, had little effect on resting membrane potential, sag potential, and rebound spike latency (inset). However, subsequent block of Ih by ZD7288 abolished the depolarizing sag and delayed the rebound spike (inset). (B) Representative traces of rebound spikes recorded in WT control conditions, with 2 µM mibefradil, and with mibefradil and 100 µM ZD7288. Here again, the T-type calcium channel blocker had little effect on resting membrane potential, sag potential, and rebound spike latency (inset), whereas ZD7288 hyperpolarized the cell, blocked the sag potential, and delayed the rebound spike. (C) Spike delay was measured as the difference between spike peaks in WT control conditions and after application of the drugs indicated below. Number of cells is indicated on the bar graph. Error bars equal +1 SD. **, P < 0.01.
