Objective: Measurement of startle response amplitude in mice exposed to acoustic stimuli to assess sound hyperresponsivity and determine whether noise-induced cochlear neuropathy results in abnormal auditory behavior
Materials & Equipment Checklist
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Equipment4
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View Abstract
Perceptual abnormalities such as hyperacusis and tinnitus often occur after acoustic overexposure. Although such exposure can also result in permanent threshold elevation, some individuals with noise-induced hyperacusis or tinnitus show clinically normal thresholds. Recent work in animals has shown that a “neuropathic” noise exposure can cause immediate, permanent degeneration of the cochlear nerve despite complete threshold recovery and lack of hair cell damage (Kujawa SG, Liberman MC. J Neurosci 29: 14077–14085, 2009; Lin HW, Furman AC, Kujawa SG, Liberman MC. J Assoc Res Otolaryngol 12: 605–616, 2011). Here we ask whether this noise-induced primary neuronal degeneration results in abnormal auditory behavior, based on the acoustic startle response (ASR) and prepulse inhibition (PPI) of startle. Responses were measured in mice exposed either to a “neuropathic” noise or to a lower-intensity, “nonneuropathic” noise and in unexposed control mice. Mice with cochlear neuropathy displayed hyperresponsivity to sound, evidenced by enhanced ASR and PPI, while exposed mice without neuronal loss showed controllike responses. Gap PPI tests, often used to assess tinnitus, revealed limited gap detection deficits in mice with cochlear neuropathy only for certain gap-startle latencies, inconsistent with the presence of tinnitus “filling in the gap.” Despite significantly reduced wave 1 of the auditory brainstem response, representing cochlear nerve activity, later peaks were unchanged or enhanced, suggesting compensatory neural hyperactivity in the auditory brainstem. Considering the rapid postexposure onset of both cochlear neuropathy and exaggerated startle-based behavior, the results suggest a role for cochlear primary neuronal degeneration, per se, in the central neural excitability that could underlie the generation of hyperacusis.
Protocol Steps
1
Noise exposure conditions
Mice were exposed to either neuropathic noise (high-intensity acoustic overexposure causing cochlear nerve degeneration) or nonneuropathic noise (lower-intensity exposure without neuronal loss), with unexposed control mice as comparison group
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Note: Neuropathic noise exposure results in immediate, permanent degeneration of cochlear nerve despite complete threshold recovery and lack of hair cell damage
View evidence from paper
“Mice were exposed either to a neuropathic noise or to a lower-intensity, nonneuropathic noise and in unexposed control mice”
2
Acoustic Startle Response (ASR) measurement
Measure startle response amplitude in mice exposed to acoustic stimuli to assess sound hyperresponsivity
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Startle Response Platform
Matches: Acoustic Startle Response (ASR) measurement system
Note: Enhanced PPI observed in mice with cochlear neuropathy compared to controls
View evidence from paper
“Mice with cochlear neuropathy displayed hyperresponsivity to sound, evidenced by enhanced ASR and PPI”
4
Gap PPI testing
Conduct gap detection tests using gap-startle latencies to assess potential tinnitus presence, as gaps in background noise may be filled in by tinnitus
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Note: Limited gap detection deficits observed only for certain gap-startle latencies in mice with cochlear neuropathy, inconsistent with tinnitus filling in the gap
View evidence from paper
“Gap PPI tests, often used to assess tinnitus, revealed limited gap detection deficits in mice with cochlear neuropathy only for certain gap-startle latencies”
5
Auditory Brainstem Response (ABR) recording
Record auditory brainstem response to measure cochlear nerve activity (wave 1) and brainstem neural activity (later peaks)
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Note: Wave 1 significantly reduced in mice with cochlear neuropathy, while later peaks unchanged or enhanced, suggesting compensatory neural hyperactivity
View evidence from paper
“Despite significantly reduced wave 1 of the auditory brainstem response, representing cochlear nerve activity, later peaks were unchanged or enhanced”
Subjects / Specimens
Species
mouse
Strain
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Age
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Sex
unknown
Weight
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Mice exposed to either neuropathic noise, nonneuropathic noise, or unexposed control mice
