Abstract：
:Subjective tinnitus may be defined as the perceptual correlate of altered spontaneous neural activity occurring in the absence of an externally evoking auditory stimulus. Tinnitus can be caused or exacerbated by one or more of five forms of stress. We propose and provide evidence supporting a model that explains, but is not limited to, peripheral (cochlear) tinnitus. In this model, naturally occurring opioid dynorphins are released from lateral efferent axons into the synaptic region beneath the cochlear inner hair cells during stressful episodes. In the presence of dynorphins, the excitatory neurotransmitter glutamate, released by inner hair cells in response to stimuli or (spontaneously) in silence, is enhanced at cochlear N-methyl-D-aspartate (NMDA) receptors. This results in altered neural excitability and/or an altered discharge spectrum in (modiolar-oriented) type I neurons normally characterized by low rates of spontaneous discharge and relatively poor thresholds. It is also possible that chronic exposure to dynorphins leads to auditory neural excitotoxicity via the same receptor mechanism. Finally, the proposed excitatory interactions of dynorphins and glutamate at NMDA receptors need not be restricted to the auditory periphery.
journal_name
Hear Resjournal_title
Hearing researchauthors
Sahley TL,Nodar RHdoi
10.1016/s0378-5955(00)00235-5keywords:
subject
Has Abstractpub_date
2001-02-01 00:00:00pages
43-54issue
1-2eissn
0378-5955issn
1878-5891pii
S0378-5955(00)00235-5journal_volume
152pub_type
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