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.