Figure 1.
Fast outward K+ currents (IK,f) are selectively abolished in IHCs from BKCa knock-out mice. A, K+ currents measured in response to depolarizing voltage steps in nominal increments of 10 mV from a holding potential of −80 mV. Recordings are from a wild-type IHC (BKα+/+; left), from a BKCa knock-out IHC (BKα−/−; middle), and from a BKα+/+ IHC in the presence of the specific BKCa blocker IbTx (100 nm; ≥10 min) in the extracellular solution (right). Recordings were made from IHCs in isolated apical turn organs of Corti at 23, 24, and 26 d after birth, respectively. B, Average steady-state current amplitudes from six BKα+/+ and 10 BKα−/− IHCs show a large reduction of overall currents. Residual currents of BKα−/− cells are equal to the IbTx-resistant currents of wild-type IHCs (n = 11). Currents are plotted against membrane potentials corrected for voltage drops across the residual series resistance (horizontal error bars). Inset, Current amplitudes at the physiological voltage range at enlarged scale. C, The background K+ current (IK,n) is not different between BKα+/+ (n = 9) and BKα−/− (n = 7) IHCs. Currents are quantified as the maximum deactivating inward tail currents at −120 mV after prepulses to voltages between −150 to −60 mV (Oliver et al., 2003). The voltage dependence of this current was also unchanged (half-activating voltage of −95.6 ± 1.7 and −99.5 ± 3.0 mV, respectively). D, Resting membrane potential in vitro is equal in BKα+/+ (n = 5) and BKα−/− (n = 8) IHCs. Symbol key in B also applies to D and E. E, Calcium currents of IHCs are not affected by ablation of BKCa. Currents through Cav channels from seven BKα+/+ and eight BKα−/− IHCs are measured with 10 mm extracellular Ba2+ as the charge carrier and with intracellular Cs+/4-AP and extracellular tetraethylammonium (10 mm) to block all K+ currents.