Tinnitus and inferior colliculus activity in chinchillas related to three distinct patterns of cochlear trauma.

A longstanding hypothesis is that tinnitus, the perception of sound without an external acoustic source, is triggered by a distinctive pattern of cochlear hair cell (HC) damage and that this subsequently leads to altered neural activity in the central auditory pathway. This hypothesis was tested by assessing behavioral evidence of tinnitus and spontaneous neural activity in the inferior colliculus (IC) after unilateral cochlear trauma. Chinchillas were assigned to four cochlear treatment groups. Each treatment produced a distinctive pattern of HC damage, as follows: acoustic exposure (AEx): sparse low-frequency inner hair cell (IHC) and outer hair cell (OHC) loss; round window cisplatin (CisEx): pronounced OHC loss mixed with some IHC loss; round window carboplatin (CarbEx): pronounced IHC loss without OHC loss; control: no loss. Compared with controls, all experimental groups displayed significant and similar psychophysical evidence of tinnitus with features resembling a 1-kHz tone. Contralateral IC spontaneous activity was elevated in the AEx and CisEx groups, which showed increased spiking and increased cross-fiber synchrony. A multidimensional analysis identified a subpopulation of neurons more prevalent in animals with tinnitus. These units were characterized by high bursting, low ISI variance, and within-burst peak spiking of approximately 1,000/sec. It was concluded that cochlear trauma in general, rather than its specific features, leads to multiple changes in central activity that underpin tinnitus. Particularly affected was a subpopulation ensemble of IC neurons with the described unique triad of features.

Acoustic injury and TRPV1 expression in the cochlear spiral ganglion.

Acoustic trauma not only produces temporary and permanent hearing loss but is a common cause of chronic tinnitus. Recent work indicated a possible role for the transient receptor potential channel vanilloid subfamily type 1 (TRPV1) in modulating the effects of cochlear injury. In our research, we investigated the effects of acoustic damage on TRPV1 expression in spiral ganglion neurons of adult rats. After exposing them unilaterally to noise, we extracted cochleas and processed the spiral ganglion for TRPV1 expression at four posttrauma intervals (2 hours, 24 hours, 12 days, and 16.9 months). We measured TRPV1 immunodensity in the apical, middle, and basal turns of the cochlea. We found a significant interaction (p = .039) between posttrauma interval and regional cochlear receptor expression: For survival intervals between 24 hours and 2 weeks, TRPV1 density increased in all cochlear regions; at the longest survival interval (16.9 months), TRPV1 density was dramatically reduced in the basal region. We also psychophysically tested the long-survival subjects, which showed evidence of 20-kHz tonal tinnitus. These results suggest that TRPV1 may participate after cochlear injury in a signal cascade that is responsible for the neuroplastic events leading to tinnitus and hyperacusis.