Auditory plasticity and hyperactivity following cochlear damage

This paper will review some of the functional changes that occur in the cen tral auditory pathway after the cochlea is damaged by acoustic overstimulat ion or by carboplatin, an ototoxic drug that selectively destroys inner hai r cells (IHCs) in the chinchilla. Acoustic trauma typically impairs the sen sitivity and tuning of auditory nerve fibers and reduces the neural output of the cochlea. Surprisingly, our results show that restricted cochlear dam age enhances neural activity in the central auditory pathway. Despite a red uction in the auditory-nerve compound action potential (CAP), the local fie ld potential from the inferior colliculus (IC) increases at a faster than n ormal rate and its maximum amplitude is enhanced at frequencies below the r egion of hearing loss. To determine if this enhancement was due to loss of sideband inhibition, we recorded from single neurons in the IC and dorsal c ochlear nucleus before and after presenting a traumatizing above the unit's characteristic frequency (CF). Following the exposure, some neurons showed substantial broadening of tuning below CF, less inhibition, and a signific ant increase in discharge rate, consistent with a model involving loss of s ideband inhibition. The central auditory system of the chinchilla can be de prived of some of its cochlear inputs by selectively destroying IHCs with c arboplatin. Selective IHC loss reduces the amplitude of the CAP without aff ecting the threshold and tuning of the remaining auditory nerve fibers. Alt hough the output of the cochlea is reduced in proportion to the amount of I HC loss. the IC response shows only a modest amplitude reduction, and remar kably, the response of the auditory cortex is enhanced. These results sugge st that the gain of the central auditory pathway can be up- or down regulat ed to compensate for the amount of neural activity from the cochlea. (C) 20 00 Elsevier Science B.V. All rights reserved.