Primary afferent dendrite degeneration as a cause of tinnitus

Abstract

Chronic tinnitus affects millions of people, but the mechanisms responsible for the development of this abnormal sensory state remain poorly understood. This study examined the type and extent of cochlear damage that occurs after acoustic trauma sufficient to induce chronic tinnitus in rats. Tinnitus was evaluated by using a conditioned suppression method of behavioral testing. Cochlear damage was assessed 6 months after acoustic trauma. There was minimal loss of inner and outer hair cells in the exposed cochleas of subjects demonstrating evidence of tinnitus. However, a significant loss of large-diameter fibers in the osseous spiral lamina of exposed cochleas of trauma subjects was observed. The significance of this finding in the context of a model of tinnitus is discussed.

Tinnitus with a Normal Audiogram: Physiological Evidence for Hidden Hearing Loss and Computational Model

“…Whether these mice also experienced tinnitus is unknown. However, in rats degeneration of AN fibers has been linked to behavioral evidence for tinnitus (Bauer et al, 2007), although these rats also suffered permanent hearing loss in the form of elevated hearing thresholds in quiet. Similarly, increased spontaneous neuronal activity has been observed in the inferior colliculus of guinea pigs (Mulders and Robertson, 2009) and in the dorsal cochlear nucleus of hamsters (Finlayson and Kaltenbach, 2009) after mild acoustic trauma that resulted in only limited hearing loss.…”

Brainstem Auditory Evoked Potentials Suggest a Role for the Ventral Cochlear Nucleus in Tinnitus

“…There were two motivations for this study. One follows from previous suggestions that tinnitus may be related to degeneration of a subset of auditory nerve fibers (ANFs) (Bauer et al 2007) and from recent animal data indicating that high-threshold ANFs may be particularly susceptible to degeneration following high-level acoustic exposures (Kujawa and Liberman 2009;Lin et al 2011). Here, the amplitude of the first ABR wave, which reflects auditory nerve activity (Buchwald and Huang 1975;Møller and Jannetta 1981), was tested for reductions in tinnitus subjects compared with closely matched non-tinnitus controls.…”

Molecular Mechanism of Tinnitus

“…In conclusion, physiological (Kaltenbach et al, 2002 ) , otoacoustic (Job et al, 2007 ) , and computational (Schaette & Kempter, 2006 ) evidence that implies that damage to OHCs may be predisposing, for tinnitus should be questioned, as previously already suggested (Bauer et al, 2007 ;Roberts et al, 2010 ) .…”

“…This would give a molecular possibility of how the discharge rate of fi bers may be altered after salicylate treatment. In contrast, other studies done on rats suggested a deafferentation of large-diameter auditory fi bers, that is, low-threshold, high-SR fi bers, after tinnitus-inducing acoustic trauma (Bauer et al, 2007 ) . A crucial future issue, therefore, is to elucidate if and how the larger size of ribbons (Liberman et al, 2011 ) , multiphasic EPSCs (Grant et al, 2010 ) , and NMDA receptors are linked with the predicted higher vulnerability of AN fi bers.…”