Abstract

The heavy metal mercury (Hg 2+) is an insidious environmental pollutant that causes toxic effects on sensory systems. It is well known that the group IIB divalent cation Hg 2+ is an inhibitor of the group I monovalent potassium (K +) cation pore-forming channel in several biological preparations. Here, we used the whole cell patch clamp technique on freshly isolated outer hair cells (OHCs) of the guinea pig cochlea to record outward K + currents and inward K + currents treated with mercuric chloride (HgCl 2). HgCl 2 affected K + currents in a voltage- and dose-dependent manner. The effects of HgCl 2 at 1.0–100 μM are more pronounced on onset peak current than on steady-state end current. HgCl 2 depolarized also the resting membrane potential. Although the effect of HgCl 2 at 1.0 μM was partially washed out over several minutes, the effects at 10 and 100 μM were irreversible to washout. Since K + channels of OHCs are targets for HgCl 2 ototoxicity, this may lead to auditory transduction problems, including a loss in hearing sensitivity. A better understanding of fundamental mechanisms underlying K + channelopathies in OHCs due to HgCl 2 poisoning may lead to better preventive or therapeutic agents.

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