Cochlear outer hair cell electromotility can provide force for both low and high intensity distortion product otoacoustic emissions

It is generally believed that the force for the otoacoustic emission (OAE) generation is provided by a mechanism of electromotility, observed in isola ted cochlear outer hair cells (OHCs). OHC electromotility is resistant to s everal ototoxic reagents, it does not depend on ATP hydrolysis, but it can be blocked by specific sulfhydryl reagents: p-chloromercuriphenylsulfonic a cid (pCMPS) and p-hydroxymercuriphenylsulfonic acid (pHMPS). We have used t hese reagents to test whether they also affect OAE. Application of pCMPS an d pHMPS on the round window membrane of anesthetized guinea pigs produced a dose-dependent inhibition of the cubic (2F(1)-F-2) distortion product OAE (DPOAE). The inhibition developed progressively from high to low frequencie s, reflecting the diffusion of the drugs through the cochlear compartment. The effect of pCMPS and pHMPS was different from the effects of furosemide and lethal anoxia, which impair cochlear function but do not block OHC elec tromotility. pHMPS suppressed DPOAE completely at all sound intensities tes ted (45-80 dB SPL), whereas furosemide or lethal anoxia caused DPOAE to dis appear at low-level stimulation (45-60 dB SPL) only. Our results suggest th at the OHC electromotility might provide the force for DPOAE generation not only at low, but also at high stimulus intensities. (C) 1998 Elsevier Scie nce B.V. All rights reserved.