Endocochlear potential and endolymphatic K+ changes induced by gap junction blockers.

OBJECTIVE

To examine the effects of gap junction blockers on the endocochlear potential (EP) and endolymphatic potassium concentration ([K(+)](e)).

METHODS

The EP and [K(+)](e) were monitored using double-barreled ion-selective microelectrodes in the second turn of the guinea pig cochlea during perilymphatic perfusion.

RESULTS

When the perilymphatic scalae of the cochlea were perfused with artificial perilymph containing 10 mM n-heptanol the EP was decreased by -8.8+/-1.4 mV (n=10), and this was accompanied by a decline in the [K(+)](e) of -6.7+/-2.1 mM (n=6). Perilymphatic application of 10 mM hexanol also produced declines in both the EP and [K(+)](e). In control studies, perilymphatic perfusion with 10 mM ethanol showed no remarkable changes in either the EP or [K(+)](e). Anoxia during perfusion with heptanol resulted in the generation of a negative EP, similar to the situation in controls.

CONCLUSIONS

A decline in the EP together with a lowering of [K(+)](e) induced by long-chain n-alkanols, which act as gap junction blockers, may be explained by an interruption in potassium ion transport related to a gap junction dysfunction.