![]() 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). Introduction: Challenges for the Investigation of the Relation between Inner Ear Injury and Auditory Cortex Plasticity These findings open new therapeutic approaches to treat the functional consequences of the cortical reorganization following cochlear damage. The cortical modifications may be reversed by treatment with antioxidants counteracting the cochlear redox imbalance. 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 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 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. ![]() 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). 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.
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