RT Journal Article SR Electronic T1 Noise-Induced Hearing Loss (NIHL) as a Target of Oxidative Stress-Mediated Damage: Cochlear and Cortical Responses after an Increase in Antioxidant Defense JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 4011 OP 4023 DO 10.1523/JNEUROSCI.2282-12.2013 VO 33 IS 9 A1 Anna Rita Fetoni A1 Paola De Bartolo A1 Sara Letizia Maria Eramo A1 Rolando Rolesi A1 Fabiola Paciello A1 Christian Bergamini A1 Romana Fato A1 Gaetano Paludetti A1 Laura Petrosini A1 Diana Troiani YR 2013 UL http://www.jneurosci.org/content/33/9/4011.abstract AB This study addresses the relationship between cochlear oxidative damage and auditory cortical injury in a rat model of repeated noise exposure. To test the effect of increased antioxidant defenses, a water-soluble coenzyme Q10 analog (Qter) was used. We analyzed auditory function, cochlear oxidative stress, morphological alterations in auditory cortices and cochlear structures, and levels of coenzymes Q9 and Q10 (CoQ9 and CoQ10, respectively) as indicators of endogenous antioxidant capability. We report three main results. First, hearing loss and damage in hair cells and spiral ganglion was determined by noise-induced oxidative stress. Second, the acoustic trauma altered dendritic morphology and decreased spine number of II–III and V–VI layer pyramidal neurons of auditory cortices. Third, the systemic administration of the water-soluble CoQ10 analog reduced oxidative-induced cochlear damage, hearing loss, and cortical dendritic injury. Furthermore, cochlear levels of CoQ9 and CoQ10 content increased. These findings indicate that antioxidant treatment restores auditory cortical neuronal morphology and hearing function by reducing the noise-induced redox imbalance in the cochlea and the deafferentation effects upstream the acoustic pathway.