Noise Overexposure Alters Long-Term Somatosensory-Auditory Processing in the Dorsal Cochlear Nucleus—Possible Basis for Tinnitus-Related Hyperactivity?
Publication Details
Featured Authors
Susanne Dehmel
Susan Shore
Journal Name
J Neuroscience
Experiment Type
Acute
Animal Model
Guinea Pig
Brain Region
Cochlear Nucleus
Brain Signal
Single Unit
NeuroNexus Category
- Penetrating Electrode
NeuroNexus Probe
- A4x4-3mm-100-125-177
Probe Detail/Package
H16_21mm
Abstract
The dorsal cochlear nucleus (DCN) is the first neural site of bimodal auditory-somatosensory integration. Previous studies have shown that
stimulation of somatosensory pathways results in immediate suppression or enhancement of subsequent acoustically evoked discharges. In the
unimpaired auditory system suppression predominates. However, damage to the auditory input pathway leads to enhancement of excitatory
somatosensory inputs to the cochlear nucleus, changing their effects on DCN neurons (Shore et al., 2008; Zeng et al., 2009).
Given the well described connection between the somatosensory system and tinnitus in patients we sought to determine whether
plastic changes in long-lasting bimodal somatosensory-auditory processing accompany tinnitus. Here we demonstrate for the first time
in vivo long-term effects of somatosensory inputs on acoustically evoked discharges of DCN neurons in guinea pigs. The effects of
trigeminal nucleus stimulation are compared between normal-hearing animals and animals overexposed with narrow band noise and
behaviorally tested for tinnitus. The noise exposure resulted in a temporary threshold shift in auditory brainstem responses but a
persistent increase in spontaneous and sound-evoked DCN unit firing rates and increased steepness of rate-level functions. Rate increases
were especially prominent in buildup units. The long-term somatosensory enhancement of sound-evoked responses was
strengthened while suppressive effects diminished in noise-exposed animals, especially those that developed tinnitus.
Damage to the auditory nerve is postulated to trigger compensatory long-term synaptic plasticity of somatosensory inputs that might
be an important underlying mechanism for tinnitus generation.
Citation
Susanne Dehmel, Shashwati Pradhan, Seth Koehler, Sanford Bledsoe, and Susan Shore. "Noise Overexposure AltersLong-TermSomatosensory-Auditory Processing in the Dorsal Cochlear Nucleus—Possible Basis
for Tinnitus-Related Hyperactivity?". The Journal of Neuroscience. (2012) 32(5):1660 –1671.
Link to Paper
Publication Date
02/ 1/2012
Country
United States
Institution
Kresge Hearing Research Institute, University of Michigan
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