title: Medial olivocochlear efferent reflex inhibition of human cochlear nerve responses.
abstract: Inhibition of cochlear amplifier gain by the medial olivocochlear (MOC) efferent system has several putative roles: aiding listening in noise, protection against damage from acoustic overexposure, and slowing age-induced hearing loss. The human MOC reflex has been studied almost exclusively by measuring changes in otoacoustic emissions. However, to help understand how the MOC system influences what we hear, it is important to have measurements of the MOC effect on the total output of the organ of Corti, i.e., on cochlear nerve responses that couple sounds to the brain. In this work we measured the inhibition produced by the MOC reflex on the amplitude of cochlear nerve compound action potentials (CAPs) in response to moderate level (52-60 dB peSPL) clicks from five, young, normal hearing, awake, alert, human adults. MOC activity was elicited by 65 dB SPL, contralateral broadband noise (CAS). Using tympanic membrane electrodes, approximately 10 h of data collection were needed from each subject to yield reliable measurements of the MOC reflex inhibition on CAP amplitudes from one click level. The CAS produced a 16% reduction of CAP amplitude, equivalent to a 1.98 dB effective attenuation (averaged over five subjects). Based on previous reports of efferent effects as functions of level and frequency, it is possible that much larger effective attenuations would be observed at lower sound levels or with clicks of higher frequency content. For a preliminary comparison, we also measured MOC reflex inhibition of DPOAEs evoked from the same ears with f2's near 4 kHz. The resulting effective attenuations on DPOAEs were, on average, less than half the effective attenuations on CAPs.
authors.affiliation: Washington University School of Medicine, Department of Otolaryngology, Saint Louis, MO 63110, USA. Electronic address: LichtenhanJ@ent.wustl.edu.
authors.forename: J T
authors.initials: JT
authors.lastname: Lichtenhan
authors.affiliation: Washington University School of Medicine, Department of Otolaryngology, Saint Louis, MO 63110, USA; Missouri State University, Communications Sciences and Disorders, Springfield, MO 65897, USA.
authors.forename: U S
authors.initials: US
authors.lastname: Wilson
authors.affiliation: Massachusetts Eye & Ear Infirmary, Eaton-Peabody Laboratory of Auditory Physiology, Boston, MA 02114, USA; Harvard Medical School, Department of Otology and Laryngology, Boston, MA 02115, USA.
authors.forename: K E
authors.initials: KE
authors.lastname: Hancock
authors.affiliation: Massachusetts Eye & Ear Infirmary, Eaton-Peabody Laboratory of Auditory Physiology, Boston, MA 02114, USA; Harvard Medical School, Department of Otology and Laryngology, Boston, MA 02115, USA.
authors.forename: J J
authors.initials: JJ
authors.lastname: Guinan
mesh_terms: D000161:Acoustic Stimulation; D001306:Auditory Pathways / Q000502:physiology; D001309:Auditory Threshold; D003051:Cochlea / Q000294:innervation*; D003056:Cochlear Nerve / Q000502:physiology*; D004525:Efferent Pathways / Q000502:physiology; D005072:Evoked Potentials, Auditory; D006801:Humans; D009433:Neural Inhibition; D009847:Olivary Nucleus / Q000502:physiology*; D017084:Otoacoustic Emissions, Spontaneous; D012018:Reflex
keywords: Cochlear amplifier; Compound action potential; Medial olivocochlear reflex; Olivocochlear efferents; Otoacoustic emissions