The effect of protein kinase C stimulator and inhibitor on cochlear potentials in the guinea pig

To determine a possible role of protein kinase C (PKC) in the cochlear, the effects of a PKC stimulator (phorbol-12-myristate-13-acetate; PMA), an inactive analogue of PKC stimulator (4 alpha-phorbol-12,13-didecanoate; 4 alpha-PDD) and a PKC inhibitor (D-sphingosine) on cochlear potentials were examined in the guinea pig. The perilymphatic perfusion with PMA (3 x 10(-6) M) produced an increase in compound action potential (CAP) amplitude and no change in N1 latency, the amplitudes of negative summating potential (-SP), cochlear microphonics (CM) and endocochlear potential (EP). The perfusion with 4 alpha-PDD (3 x 10(-6) M) did not change the sound-evoked cochlear potentials and the EP. The perfusion with D-sphingosine (10(-5) M) produced a decrease in CAP amplitude and no change in N1 latency and the amplitudes of -SP, CM and EP. The results suggest that PKC may be involved in the mechanism underlying the CAP generation.