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

• Published in: Hearing research 1998-12, Vol.126 (1), p.67-74
• Main Authors: Frolenkov, Gregory I, Belyantseva, Inna A, Kurc, Mauricio, Mastroianni, Mary Ann, Kachar, Bechara
• Format: Article
• Language: English
• Subjects: 4-Chloromercuribenzenesulfonate - pharmacology; Animals; Biological and medical sciences; Cell Movement - physiology; Cochlea - cytology; Cochlea - physiology; Cochlear amplifier; Ear and associated structures. Auditory pathways and centers. Hearing. Vocal organ. Phonation. Sound production. Echolocation; Electrophysiology; Female; Fundamental and applied biological sciences. Psychology; Furosemide - pharmacology; Guinea pig; Guinea Pigs; Hair Cells, Auditory, Outer - physiology; Hypoxia - physiopathology; Male; Otoacoustic emission; Otoacoustic Emissions, Spontaneous - drug effects; Otoacoustic Emissions, Spontaneous - physiology; Outer hair cell motility; Oxidants - pharmacology; Phenylmercury Compounds - pharmacology; Sulfhydryl Compounds - pharmacology; Sulfhydryl reagent; Vertebrates: nervous system and sense organs
• ISSN: 0378-5955; 1878-5891
• DOI: 10.1016/S0378-5955(98)00150-6

It is generally believed that the force for the otoacoustic emission (OAE) generation is provided by a mechanism of electromotility, observed in isolated cochlear outer hair cells (OHCs). OHC electromotility is resistant to several ototoxic reagents, it does not depend on ATP hydrolysis, but it can be blocked by specific sulfhydryl reagents: p-chloromercuriphenylsulfonic acid (pCMPS) and p-hydroxymercuriphenylsulfonic acid (pHMPS). We have used these reagents to test whether they also affect OAE. Application of pCMPS and pHMPS on the round window membrane of anesthetized guinea pigs produced a dose-dependent inhibition of the cubic (2 F 1− F 2) distortion product OAE (DPOAE). The inhibition developed progressively from high to low frequencies, 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 electromotility. pHMPS suppressed DPOAE completely at all sound intensities tested (45–80 dB SPL), whereas furosemide or lethal anoxia caused DPOAE to disappear at low-level stimulation (45–60 dB SPL) only. Our results suggest that the OHC electromotility might provide the force for DPOAE generation not only at low, but also at high stimulus intensities.