Supporting cells of Corti's organ are electrically coupled via gap junction
s. They probably serve to maintain the unique cochlear environment that is
required for normal sensory function. In this study we used input capacitan
ce measurements under whole-cell voltage-clamp conditions to evaluate the e
ffects of nitric oxide on gap junctional communication between pairs of iso
lated supporting Deiters cells. We show that the nitric oxide (NO) donor so
dium nitroprusside causes the uncoupling of Deiters cells, and that an NO s
ynthase inhibitor blocks the effect. The cGMP analogue 8-bromo-cGMP also un
couples Deiters cells. With either treatment, the input capacitance of pair
s of Deiters cells drops to single-cell levels within minutes of applicatio
n, indicative of electrical uncoupling. We surmise that the NO/cGMP pathway
may serve to modulate normal cochlear homeostasis and possibly plays a rol
e in ototoxic mechanisms.