Contralateral Inhibition of Click- and Chirp-Evoked Human Compound Action Potentials.

Spencer B Smith,Barbara K Cone,Jeffery T Lichtenhan

doi:10.3389/fnins.2017.00189

Spencer B Smith, Barbara K Cone + Show 1 more

Open Access

https://doi.org/10.3389/fnins.2017.00189

Copy DOI

Abstract

Cochlear outer hair cells (OHC) receive direct efferent feedback from the caudal auditory brainstem via the medial olivocochlear (MOC) bundle. This circuit provides the neural substrate for the MOC reflex, which inhibits cochlear amplifier gain and is believed to play a role in listening in noise and protection from acoustic overexposure. The human MOC reflex has been studied extensively using otoacoustic emissions (OAE) paradigms; however, these measurements are insensitive to subsequent “downstream” efferent effects on the neural ensembles that mediate hearing. In this experiment, click- and chirp-evoked auditory nerve compound action potential (CAP) amplitudes were measured electrocochleographically from the human eardrum without and with MOC reflex activation elicited by contralateral broadband noise. We hypothesized that the chirp would be a more optimal stimulus for measuring neural MOC effects because it synchronizes excitation along the entire length of the basilar membrane and thus evokes a more robust CAP than a click at low to moderate stimulus levels. Chirps produced larger CAPs than clicks at all stimulus intensities (50–80 dB ppeSPL). MOC reflex inhibition of CAPs was larger for chirps than clicks at low stimulus levels when quantified both in terms of amplitude reduction and effective attenuation. Effective attenuation was larger for chirp- and click-evoked CAPs than for click-evoked OAEs measured from the same subjects. Our results suggest that the chirp is an optimal stimulus for evoking CAPs at low stimulus intensities and for assessing MOC reflex effects on the auditory nerve. Further, our work supports previous findings that MOC reflex effects at the level of the auditory nerve are underestimated by measures of OAE inhibition.

Highlights

Cochlear outer hair cells (OHC) receive direct efferent feedback from the caudal auditory brainstem via the medial olivocochlear (MOC) nerve bundle
Because otoacoustic emissions (OAEs) likely originate from mechanics associated with OHC motility (Liberman et al, 2002; Cheatham et al, 2004; Dallos et al, 2008), they are sensitive to MOC reflex-induced changes in OHC function and provide a non-invasive, albeit indirect, method to study efferent effects in humans
Note that clickevoked responses at 50 dB peak-to-peak equivalent sound pressure level (ppeSPL) were separable from the noise floor in all three test sessions in only 9 of the 14 participants; amplitude ratios were calculated for only 9 participants at this level

Summary

Introduction

Cochlear outer hair cells (OHC) receive direct efferent feedback from the caudal auditory brainstem via the medial olivocochlear (MOC) nerve bundle. Magnitude and/or phase differences between OAEs recorded without and with CAS are used to quantify MOC reflex-induced shifts in OHC function (Guinan, 2006). Such studies have quantified characteristics of human MOC reflex strength (e.g., Backus and Guinan, 2007; Marshall et al, 2014), tuning (e.g., Veuillet et al, 1991; Chéry-Croze et al, 1993; Lilaonitkul and Guinan, 2009; Zhao and Dhar, 2012), and laterality (e.g., Francis and Guinan, 2010; Garinis et al, 2011). OAEs are pre-neural measurements and are less informative about the “downstream” MOC effects on IHC excitation and the subsequent neural ensembles that mediate hearing

Methods

Results

Discussion

Conclusion