Endolymphatic sodium homeostasis by Reissner's membrane

Cochlear sensory transduction depends on active extrusion of sodium ion (Na(+)) from the luminal fluid, endolymph. Reissner's membrane epithelium forms much of the barrier between cochlear endolymph and perilymph and we hypothesized that Reissner's membrane might be responsible for this function. We found that Reissner's membrane isolated from gerbil produced a short circuit current (I(sc)) directed into the apical side, consistent with cation absorption and/or anion secretion. I(sc) was inhibited by amiloride analogs in the potency sequence benzamil>amiloride>>ethylisopropylamiloride, consistent with Na(+) absorption through an epithelial sodium channel in the apical cell membrane. I(sc) was also inhibited by an inhibitor of Na(+),K(+)-ATPase, ouabain, and by the K(+) channel blockers Ba(2+), 4-aminopyridine and quinine but not tetraethylammonium nor glibenclamide, consistent with the presence of a voltage-activated K(+) channel. Bumetanide, an inhibitor of the Na(+),2Cl(-),K(+)-cotransporter, had no effect on I(sc). Contrary to previous hypotheses, no evidence was found for electrogenic secretion of Cl(-) under control of cAMP since neither forskolin nor genistein affected I(sc) when Na(+) absorption was blocked. These results provide the first direct evidence that Reissner's membrane contributes to normal cochlear function by absorption of Na(+) from endolymph.