Dorsal cochlear nucleus responses to somatosensory stimulation are enhanced after noise-induced hearing loss

Eur J Neurosci. 2008 Jan;27(1):155-68. doi: 10.1111/j.1460-9568.2007.05983.x.


Multisensory neurons in the dorsal cochlear nucleus (DCN) achieve their bimodal response properties [Shore (2005) Eur. J. Neurosci., 21, 3334-3348] by integrating auditory input via VIIIth nerve fibers with somatosensory input via the axons of cochlear nucleus granule cells [Shore et al. (2000) J. Comp. Neurol., 419, 271-285; Zhou & Shore (2004)J. Neurosci. Res., 78, 901-907]. A unique feature of multisensory neurons is their propensity for receiving cross-modal compensation following sensory deprivation. Thus, we investigated the possibility that reduction of VIIIth nerve input to the cochlear nucleus results in trigeminal system compensation for the loss of auditory inputs. Responses of DCN neurons to trigeminal and bimodal (trigeminal plus acoustic) stimulation were compared in normal and noise-damaged guinea pigs. The guinea pigs with noise-induced hearing loss had significantly lower thresholds, shorter latencies and durations, and increased amplitudes of response to trigeminal stimulation than normal animals. Noise-damaged animals also showed a greater proportion of inhibitory and a smaller proportion of excitatory responses compared with normal. The number of cells exhibiting bimodal integration, as well as the degree of integration, was enhanced after noise damage. In accordance with the greater proportion of inhibitory responses, bimodal integration was entirely suppressive in the noise-damaged animals with no indication of the bimodal enhancement observed in a sub-set of normal DCN neurons. These results suggest that projections from the trigeminal system to the cochlear nucleus are increased and/or redistributed after hearing loss. Furthermore, the finding that only neurons activated by trigeminal stimulation showed increased spontaneous rates after cochlear damage suggests that somatosensory neurons may play a role in the pathogenesis of tinnitus.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acoustic Stimulation / methods
  • Action Potentials / physiology
  • Animals
  • Auditory Pathways / physiology
  • Cochlear Nucleus / pathology*
  • Cochlear Nucleus / physiopathology*
  • Disease Models, Animal
  • Electric Stimulation / methods
  • Evoked Potentials, Auditory, Brain Stem / physiology*
  • Evoked Potentials, Auditory, Brain Stem / radiation effects
  • Female
  • Guinea Pigs
  • Hearing Loss, Noise-Induced / pathology*
  • Models, Neurological
  • Neural Inhibition / physiology
  • Neurons
  • Noise / adverse effects
  • Principal Component Analysis
  • Reaction Time / physiology
  • Sensory Thresholds / physiology
  • Trigeminal Nerve / physiology