Mechanisms of synaptic plasticity in the dorsal cochlear nucleus: plasticity-induced changes that could underlie tinnitus

Am J Audiol. 2008 Dec;17(2):S170-5. doi: 10.1044/1059-0889(2008/07-0030). Epub 2008 Oct 31.


Purpose: Tinnitus is the persistent perception of a subjective sound. Tinnitus is almost universally experienced in some forms. In most cases, recovery may occur in seconds, hours, or days. How does tinnitus shift from a transient condition to a lifelong disorder? Several lines of evidence, including clinical studies and animal models, indicate that the brain, rather than the inner ear, may in some cases be the site of maintenance of tinnitus. One hypothesis is that normal electrical activity in the auditory system becomes pathologically persistent due to plasticity-like mechanisms that can lead to long-term changes in the communication between neurons. A candidate site for the expression of this so-called synaptic plasticity is a region of the brainstem called the dorsal cochlear nucleus (DCN), a site of integration of acoustic and multimodal, sensory inputs.

Conclusions: Here we review recent findings on cellular mechanisms observed in the DCN that can lead to long-term changes in the synaptic strength between different neurons in the DCN. These cellular mechanisms could provide candidate signaling pathways underlying the induction (ignition) and/or the expression (maintenance) of tinnitus.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Auditory Pathways / physiopathology
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2 / physiology
  • Chronic Disease
  • Cochlear Nucleus / physiopathology*
  • Humans
  • Long-Term Potentiation / physiology
  • Nerve Net / physiopathology
  • Neuronal Plasticity / physiology*
  • Receptor, Cannabinoid, CB1 / physiology
  • Receptors, AMPA / physiology
  • Receptors, N-Methyl-D-Aspartate / physiology
  • Signal Transduction / physiology
  • Synapses / physiology*
  • Tinnitus / physiopathology*


  • Receptor, Cannabinoid, CB1
  • Receptors, AMPA
  • Receptors, N-Methyl-D-Aspartate
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2