Auditory plasticity and hyperactivity following cochlear damage.

摘要: This paper will review some of the functional changes that occur in central auditory pathway after cochlea is damaged by acoustic overstimulation or carboplatin, an ototoxic drug selectively destroys inner hair cells (IHCs) chinchilla. Acoustic trauma typically impairs sensitivity and tuning nerve fibers reduces neural output cochlea. Surprisingly, our results show restricted cochlear damage enhances activity pathway. Despite a reduction auditory-nerve compound action potential (CAP), local field from inferior colliculus (IC) increases at faster than normal rate its maximum amplitude enhanced frequencies below region hearing loss. To determine if this enhancement was due to loss sideband inhibition, we recorded single neurons IC dorsal nucleus before presenting traumatizing above unit's characteristic frequency (CF). Following exposure, showed substantial broadening CF, less significant increase discharge rate, consistent with model involving inhibition. The system chinchilla can be deprived inputs destroying IHCs carboplatin. Selective IHC CAP without affecting threshold remaining fibers. Although reduced proportion amount loss, response shows only modest reduction, remarkably, cortex enhanced. These suggest gain up- down regulated compensate for