Effects of nimodipine, an L-type calcium channel antagonist, on the chicken's cochlear potentials

At most synapses in the brain, neurotransmitter release depends on N-type or P/Q-type calcium channels. However, available in vitro experimental data suggest that there exist almost exclusively L-type calcium channels in sensory hair cells of most species. To test whether chicken hair cells depend on L-type calcium channels for neurotransmitter release, we examined the effects of nimodipine, a selective L-type calcium channel antagonist, on acoustically evoked cochlear potentials in 10-15 week old chickens in vivo. Diffusion of nimodipine into scala tympani significantly elevated threshold, dramatically decreased the amplitude and increased the latency of the compound action potential within 20 min of drug application. The summating potential was also significantly reduced in amplitude, but the cochlear microphonic was relatively less affected. All the effects were reversible after nimodipine was washed out with artificial perilymph except that the cochlear microphonic amplitude remained decreased. Application of omega-conotoxin GVIA, an N-type calcium channel antagonist and agatoxin Tk, a P-type calcium channel antagonist had no observable effects on the cochlear potentials. These results suggest that L-type calcium channels control neurotransmitter release from avian hair cells.