Abstract

Over the last decade, the consequences of acoustic trauma on the functional properties of auditory cortex neurons have received growing attention. Changes in spontaneous and evoked activity, shifts of characteristic frequency (CF), and map reorganizations have extensively been described in anesthetized animals (e.g., Noreña and Eggermont, 2003, 2005). Here, we examined how the functional properties of cortical cells are modified after partial hearing loss in awake guinea pigs. Single unit activity was chronically recorded in awake, restrained, guinea pigs from 3 days before up to 15 days after an acoustic trauma induced by a 5 kHz 110 dB tone delivered for 1 h. Auditory brainstem responses (ABRs) audiograms indicated that these parameters produced a mean ABR threshold shift of 20 dB SPL at, and one octave above, the trauma frequency. When tested with pure tones, cortical cells showed on average a 25 dB increase in threshold at CF the day following the trauma. Over days, this increase progressively stabilized at only 10 dB above control value indicating a progressive recovery of cortical thresholds, probably reflecting a progressive shift from temporary threshold shift (TTS) to permanent threshold shift (PTS). There was an increase in response latency and in response variability the day following the trauma but these parameters returned to control values within 3 days. When tested with conspecific vocalizations, cortical neurons also displayed an increase in response latency and in response duration the day after the acoustic trauma, but there was no effect on the average firing rate elicited by the vocalization. These findings suggest that, in cases of moderate hearing loss, the temporal precision of neuronal responses to natural stimuli is impaired despite the fact the firing rate showed little or no changes.

Highlights

  • If neuronal activity is collected shortly after hearing loss, it will reveal a neuronal correlate of temporary threshold shift (TTS), whereas recording neural activity months after hearing loss will reveal a correlate of permanent threshold shift (PTS) with a potential contribution of functional reorganizations occurring at the cortical and subcortical levels

  • EVALUATION OF THE HEARING DEFICIT BY Auditory brainstem responses (ABRs) Since we did not record the ABRs of our animals (n = 10) before and after the acoustic trauma, hearing loss evaluation is only based on ABRs obtained a few weeks after the last recording session

  • We compared the ABRs obtained from our hearing impaired animals with a large database of ABRs obtained in control guinea pigs (n = 46) of the same age (4.7 ± 0.6 months) and weight (585 ± 113 g) than the ones used here

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Summary

Introduction

An increasing number of studies have described the reorganizations occurring in the adult auditory system after partial hearing loss performed either by traumatic noise or by partial lesions of the cochlea (e.g., Robertson and Irvine, 1989; Kamke et al, 2003; Noreña and Eggermont, 2003, 2005; Rosen et al, 2012). Electrophysiological studies have documented that exposure to loud, traumatic sounds generating partial hearing loss produced alterations in frequency tuning (Rajan, 1998, 2001; Kimura and Eggermont, 1999; Noreña and Eggermont, 2003; Scholl and Wehr, 2008; Gourévitch and Edeline, 2011) and tonotopic map reorganizations (Noreña and Eggermont, 2005) These changes in functional properties may result both from physiological modifications already occurring at subcortical levels (Wang et al, 1996, 2002; Kamke et al, 2003; Vale et al, 2003) and/or from morphological alterations of cortical cells such as modifications in dendritic morphology and in dendritic spine numbers (Fetoni et al, 2013). If neuronal activity is collected shortly after hearing loss, it will reveal a neuronal correlate of temporary threshold shift (TTS), whereas recording neural activity months after hearing loss will reveal a correlate of permanent threshold shift (PTS) with a potential contribution of functional reorganizations occurring at the cortical and subcortical levels

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