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.