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Hear Res. 2013 Jan;295:124-9. doi: 10.1016/j.heares.2012.02.002. Epub 2012 Feb 13.

Spontaneous hyperactivity in the auditory midbrain: relationship to afferent input.

Author information

1
The Auditory Laboratory, School of Anatomy, Physiology and Human Biology, M311, The University of Western Australia, 35 Stirling hwy, Crawley, Western Australia 6009, Australia. don.robertson@uwa.edu.au

Abstract

Hyperactivity in the form of increased spontaneous firing rates of single neurons develops in the guinea pig inferior colliculus (IC) after unilateral loud sound exposures that result in behavioural signs of tinnitus. The hyperactivity is found in those parts of the topographic frequency map in the IC where neurons possess characteristic frequencies (CFs) closely related to the region in the cochlea where lasting sensitivity changes occur as a result of the loud sound exposure. The observed hyperactivity could be endogenous to the IC, or it could be driven by hyperactivity at lower stages of the auditory pathway. In addition to the dorsal cochlear nucleus (DCN) hyperactivity reported by others, specific cell types in the ventral cochlear nucleus (VCN) also show hyperactivity in this animal model suggesting that increased drive from several regions of the lower brainstem could contribute to the observed hyperactivity in the midbrain. In addition, spontaneous afferent drive from the cochlea itself is necessary for the maintenance of hyperactivity up to about 8 weeks post cochlear trauma. After 8 weeks however, IC hyperactivity becomes less dependent on cochlear input, suggesting that central neurons transition from a state of hyperexcitability to a state in which they generate their own endogenous firing. The results suggest that there might be a "therapeutic window" for early-onset tinnitus, using treatments that reduce cochlear afferent firing.

PMID:
22349094
DOI:
10.1016/j.heares.2012.02.002
[Indexed for MEDLINE]

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