Salicylate's Effects on Cochlear Sensitivity and Sound Processing in Primary Auditory Cortex of the Rat
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Tinnitus is a disorder of the auditory system which is characterized by the persistent perception of a sound (most commonly a ringing or hissing noise) in the absence of an acoustic source in the environment. Research in humans and animal models of tinnitus indicate that hearing loss likely serves as a triggering event for neuroplastic changes within the brain resulting in aberrant neural activity which is perceived as a phantom sound. In particular, the primary auditory cortex (AC) has been shown to be hyper-responsive to sound in both humans with tinnitus and animal models of tinnitus. The abnormal activation of neural circuits underlying this hyper-responsivity of AC to sound indicates that the brain may be more permissive to aberrant patterns of spontaneous neural activity which generates the tinnitus perception. The experiments described herein investigated changes in cochlear sensitivity and neural activity in primary AC in a rat model of salicylate-induced tinnitus. Measures were made of cochlear sensitivity and neural activity in primary AC was characterized following a high dose of sodium salicylate; a drug which at high doses reliably induces tinnitus in humans and rats. Results from these experiments corroborate and extend a model of tinnitus whereby the profile of hearing loss following a high dose of sodium salicylate likely contributes to determining the pitch of the tinnitus percept. Furthermore, neural activity within primary AC is altered resulting in hyper-responsivity and further amplification of neural activity via intracortical pathways residing in the superficial layers of cortex.