More Research on Lateral Inhibition
An interesting paper reveals a little bit more about the relationship between abnormal lateral inhibition and tinnitus. The abstract is a bit opaque:
Tinnitus is likely initiated by a discontinuity in the spontaneous or low-level-stimulus induced neural activity across auditory nerve fibers with different characteristic frequency (CF). This discontinuity may be caused by functional loss of outer hair cells in those regions where inner hair cells are preserved.
The reduced spontaneous activity for nerve fibers with CFs in the hearing loss range may result in a reduction of lateral inhibition at more central levels. This reduced lateral inhibition of neurons with CFs close to the edge frequency of the audiogram induces hypersensitivity and hyperactivity in these neurons.
Persistent changes in lateral inhibition result in increased numbers of neurons that are tuned to a limited range of frequencies at the edge of the cochlear lesion. Thus, the frequency map in auditory cortex, the tonotopic map, becomes reorganized as it reflects these changes.
The spontaneous neuronal firings in the auditory cortex after insults that cause tinnitus show increased synchrony, thereby mimicking one aspect of the responses to normal sound stimulation. All long-standing tinnitus may thus be called central tinnitus, despite the fact that it is initiated by cochlear hearing loss or is localized to the hearing loss ear.