Outer hair cells (OHC) serve as electromechanical amplifiers that guarantee the unique sensitivity and frequency selectivity of the mammalian cochlea. It is unknown whether the afferent fibres connected to adult OHCs are functional. If so, voltage‐activated Ca2+ channels would be required for afferent synaptic transmission. In neonatal OHCs, Ca2+ channels seem to play a role in maturation since OHCs from Cav1.3‐deficient (Cav1.3−/−) mice degenerate shortly after the onset of hearing. We therefore studied whole‐cell Ca2+ currents in outer hair cells aged between postnatal day 1 (P1) and P8. OHCs showed a rapidly activating inward current that was 1.8 times larger with 10 mm Ba2+ as charge carrier (IBa) than with equimolar Ca2+ (ICa). IBa started activating at −50 mV with Vmax=−1.9 ± 6.9 mV, V0.5=−15.0 ± 7.1 mV and k= 8.2± 1.1 mV (n= 34). The peak IBa showed negligible inactivation (3.6 % after 300 ms) whereas the ICa (10 mm Ca2+) was inactivated by 50.7 %. OHC IBa was reduced by 33.5 ± 10.3 % (n= 14) with 10 μm nifedipine and increased to 178.5 ± 57.8 % (n= 14) by 5 μm Bay K 8644. A dose‐response curve for nifedipine revealed an IC50 of 2.3 μm, a Hill coefficient of 2.7 and a maximum block of 36 %. Average IBa density in OHCs was 24.4 ± 10.8 pA pF−1 (n= 105) which is only 38 % of the value in inner hair cells. Single cell RT‐PCR revealed expression of Cav1.3 in OHCs. In OHCs from Cav1.3−/− mice, Ba2+ current density was reduced to 0.6 ± 0.5 pA pF−1 (n= 9) indicating that > 97 % of the Ca2+ channel current in OHCs flows through Cav1.3.

Adult inner hair cells (IHCs) possess voltage-activated Ca2+ currents that couple receptor potentials to transmitter release at the afferent synapses. Before the onset of hearing both IHCs and outer hair cells (OHCs) exhibit Ca2+ currents. More than 90% of neonatal hair cell (HC) currents flow through alpha1D Ca2+ channel subunits because they are absent in both IHCs and OHCs from alpha1D-/- mice and residual currents are insensitive to L-type agonists. Since lack of the alpha1D-subunit leads to HC degeneration and profound deafness, class D L-type Ca2+ currents seem to be crucial for the development and functioning of the inner ear. Neonatal HC Ca2+ currents were studied using the whole-cell patch clamp technique. They showed rapid activation, rapid deactivation and very little inactivation. They started activating as negative as -65mV. In contrast to alpha1C-mediated (classical L-type) Ca2+ currents, they showed a rather low sensitivity to various L-type antagonists. 10 microM nifedipine e.g. blocked HC Ca2+ currents by about 40% whereas class C L-type Ca2+ currents are completely blocked by 100nM nifedipine. The L-type channel agonist Bay K 8644 increased the HC Ca2+ current by 100-200% and shifted the IV curve to more negative potentials which is similar to its effects in alpha1C-mediated Ca2+ currents.