Electrically Evoked Medial Olivocochlear Efferent Effects on Stimulus Frequency Otoacoustic Emissions in Guinea Pigs

• Published in: Journal of the Association for Research in Otolaryngology Vol. 18; no. 1; pp. 153 - 163
• Main Authors: Berezina-Greene, Maria A., Guinan, John J.
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.02.2017; Springer Nature B.V
• Subjects: Acoustic Stimulation; Animals; Cochlea - physiology; Efferent Pathways - physiology; Guinea Pigs; Medicine; Medicine & Public Health; Neurobiology; Neurosciences; Olivary Nucleus - physiology; Otoacoustic Emissions, Spontaneous - physiology; Otorhinolaryngology; Research Article; Cochlear irregularities; SFOAE; Cochlear mechanics; Medial olivocochlear
• ISSN: 1525-3961; 1438-7573
• DOI: 10.1007/s10162-016-0593-5

Stimulus frequency otoacoustic emissions (SFOAEs) are produced by cochlear irregularities reflecting energy from the peak region of the traveling wave (TW). Activation of medial olivocochlear (MOC) efferents reduces cochlear amplification and otoacoustic emissions (OAEs). In other OAEs, MOC activation can produce enhancements. The extent of MOC enhancements of SFOAEs has not been previously studied. In anesthetized guinea pigs, we electrically stimulated MOC fibers and recorded their effects on SFOAEs. MOC stimulation mostly inhibited SFOAEs but sometimes enhanced them. Some enhancements were not near response dips and therefore cannot be explained by a reduction of wavelet cancelations. MOC stimulation always inhibited auditory-nerve compound action potentials showing that cochlear-amplifier gain was not increased. We propose that some SFOAE enhancements arise because shocks excite only a small number of MOC fibers that inhibit a few scattered outer hair cells thereby changing (perhaps increasing) cochlear irregularities and SFOAE amplitudes. Contralateral sound activation is expected to excite approximately one third of MOC efferents and may also change cochlear irregularities. Some papers suggest that large SFOAE components originate far basal of the TW peak, basal of the region that receives cochlear amplification. Using a time-frequency analysis, we separated SFOAEs into components with different latencies. At all SFOAE latencies, most SFOAE components were inhibited by MOC stimulation, but some were enhanced. The MOC inhibition of short-latency SFOAE components is consistent with these components being produced in the cochlear-amplified region near the TW peak.