INVOLVEMENT OF CL- TRANSPORT IN FORSKOLIN-INDUCED ELEVATION OF ENDOCOCHLEAR POTENTIAL

To determine the possible involvement of C1(-) transport in the forsko lin-induced endocochlear potential (EP) elevation, the effect of forsk olin on the EP was examined in C1(-)-free artificial perilymph (aPL) a s well as in the presence of Cl- channel blockers. The perfusion of sc ala vestibuli (SV) with forskolin (200 mu M) dissolved in Cl--free aPL failed to produce an EP elevation, while SV perfusion of forskolin di ssolved in normal aPL elevated the EP. The application of DPC and IAA- 94 (blockers of cAMP-activated Cl- channel) into SV completely suppres sed the forskolin-induced EP elevation, while niflumic acid (a Ca2+-ac tivated Cl- channel blocker) failed to do so. IAA-94 applied into scal a tympani (ST) did not suppress this EP elevation. The results suggest that adenylate cyclase may modulate the EP by changing Cl- transport between SV and scala media (SM) across Reissner's membrane.