Salicylate's Effects on Cochlear Sensitivity and Sound Processing in Primary Auditory Cortex of the Rat.

摘要

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.