Cochlear injury and adaptive plasticity of the auditory cortex.

Anna Rita Fetoni,Gaetano Paludetti,Laura Petrosini,Diana Troiani

doi:10.3389/fnagi.2015.00008

Abstract

Growing evidence suggests that cochlear stressors as noise exposure and aging can induce homeostatic/maladaptive changes in the central auditory system from the brainstem to the cortex. Studies centered on such changes have revealed several mechanisms that operate in the context of sensory disruption after insult (noise trauma, drug-, or age-related injury). The oxidative stress is central to current theories of induced sensory-neural hearing loss and aging, and interventions to attenuate the hearing loss are based on antioxidant agent. The present review addresses the recent literature on the alterations in hair cells and spiral ganglion neurons due to noise-induced oxidative stress in the cochlea, as well on the impact of cochlear damage on the auditory cortex neurons. The emerging image emphasizes that noise-induced deafferentation and upward spread of cochlear damage is associated with the altered dendritic architecture of auditory pyramidal neurons. The cortical modifications may be reversed by treatment with antioxidants counteracting the cochlear redox imbalance. These findings open new therapeutic approaches to treat the functional consequences of the cortical reorganization following cochlear damage.

Highlights

CHALLENGES FOR THE INVESTIGATION OF THE RELATION BETWEEN INNER EAR INJURY AND AUDITORY CORTEX PLASTICITY Sensory-neural hearing loss is a disorder surprisingly frequent in the general population (Nelson et al, 2005) affecting severely the quality of life as reported by several assessments (Seidman and Standring, 2010)
Mitochondrial production of reactive oxygen species (ROS) is central to the free radical theory of aging (Lenaz, 2012; Orr et al, 2013). This theory has been implicated in the pathogenesis of virtually all age-associated diseases as well as in noise-induced hearing loss (NIHL), the second most common sensory-neural hearing deficit after agerelated hearing loss (Van Eyken et al, 2007; Someya et al, 2009; Fetoni et al, 2011)
The current review will examine the convergence of factors related to auditory insults from a bottom-up perspective, coupling the acoustically- or aging-induced functional changes at peripheral level [e.g., hearing receptor and spiral ganglion neuron (SGN) function] with the central changes at the level of the pyramidal neurons in the auditory cortices

Summary

Cochlear injury and adaptive plasticity of the auditory cortex

Edited by: Isabel Varela-Nieto, Consejo Superior de Investigaciones Científicas, Spain. Growing evidence suggests that cochlear stressors as noise exposure and aging can induce homeostatic/maladaptive changes in the central auditory system from the brainstem to the cortex. Studies centered on such changes have revealed several mechanisms that operate in the context of sensory disruption after insult (noise trauma, drug-, or age-related injury). The present review addresses the recent literature on the alterations in hair cells and spiral ganglion neurons due to noise-induced oxidative stress in the cochlea, as well on the impact of cochlear damage on the auditory cortex neurons. The cortical modifications may be reversed by treatment with antioxidants counteracting the cochlear redox imbalance These findings open new therapeutic approaches to treat the functional consequences of the cortical reorganization following cochlear damage

INTRODUCTION

Cortical modifications following cochlear damage

CONCLUSION