Changes in the adult chinchilla cochlear nucleus following acoustic trauma

Date of Completion

January 1999


Health Sciences, Audiology|Biology, Neuroscience




Hearing loss and abnormal auditory function, including tinnitus, are common events after exposure to very loud noises in humans, although little is known of their causes. The present study addresses the nature and underlying mechanisms of changes in the cochlear nucleus (CN) of adult chinchillas following noise trauma. Chinchillas have a similar hearing range as humans and provide a useful model, as noise exposure causes damage to hair cells and sensory nerve fibers in the cochlea, followed by degeneration of axons and synaptic endings in the CN, and eventually by the growth of axons. In the present study, following a single unilateral exposure to an octave-band noise centered at 4 kHz, at an intensity of 108 dB SPL, synaptophysin immunostaining was used to assess changes in the number of synaptic endings, D-[3H]aspartate and [14C]glycine release and uptake and [3H]AMPA and [3H]strychnine binding were used to assess transmitter activities in the CN. ^ In the ipsilateral CN, a gradual decrease in the number of synaptophysin-positive objects persisted throughout the timecourse, although a transient increase occurred at 90 days. Glutamatergic synaptic transmission was initially increased, but both glutamatergic and glycinergic transmission was decreased by 14 days, when axonal degeneration was evident, and recovered by 90 days. ^ In the contralateral CN, striking decreases were evident in synaptophysin immunostaining by 7 days which persisted in the absence of axonal degeneration, suggesting an induction by signals from the ipsilateral side. Transient changes in transmission returned to control levels by 90 days. ^ The findings suggest that a series of plastic events occurred in the CN of the adult chinchilla after noise exposure which may lead to changes in the number of synapses and the regulation of axonal endings that use glutamate or glycine for synaptic transmission. The changes were more widespread than predicted by the extent of cochlear damage, suggesting that peripheral damage and/or overstimulation unleash signals that spread in the central auditory pathways to effect changes in transmission and the balance of excitatory and inhibitory processes. This opens up the prospect of future drug therapies that address such imbalances. ^