Hearing research
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High rate intracochlear electrical stimulation at high intensities can induce significant reductions in the excitability of the auditory nerve as measured by a decrement in the amplitude of the electrically evoked auditory brainstem response (EABR). Such changes are primarily associated with stimulus induced neuronal activity, although direct current (DC) can also contribute. We examined the extent of stimulus induced change in auditory nerve excitability using large surface area platinum electrodes ('high-Q' electrodes). ⋯ However, EABRs were reduced significantly at 400 and 1000 pps. There was significantly greater EABR recovery following stimulation using high-Q electrodes compared with standard Pt electrodes at 400 (P<0.05) and 1000 pps (P<0.05). These data indicate that large surface area electrodes can significantly reduce stimulus induced changes in auditory nerve excitability, and may therefore have important clinical application.
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Latency, temporal dispersion and input-output characteristics of auditory nerve fiber responses to electrical pulse trains in normal and chronically deafened cat ears were classified and tentatively associated with sites where activity is initiated. Spikes occurred in one or more of four discrete time ranges whose endpoints overlapped partially. A responses had latencies <0.44 ms, exhibited asymptotic temporal dispersion of 8-12 micros and possessed an average dynamic range of 1.2 dB for 200 pulses/s (pps) pulse trains. ⋯ Responses to high-rate stimuli also exhibited discrete latency increases when discharge rates exceeded 300-400 spikes/s. Spike by spike latencies in these cases depended strongly on the discharge history. Implications for high-rate speech processing strategies are discussed.
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We examined the effect of a neonatal sensorineural hearing loss on the soma area of neurones in the central nucleus of the inferior colliculus (ICC) in adult cats to evaluate the role of auditory experience on neuronal atrophy within the auditory midbrain. Three groups of animals were used: bilaterally deafened, unilaterally deafened and normal hearing controls. ⋯ In contrast, there was no significant difference in mean soma area between normal hearing and unilaterally deafened animals (P0.05) irrespective of whether the ICC examined was ipsi- or contralateral to the deafened ear. These results demonstrate that the reduction in soma area of auditory brainstem neurones reported following a sensorineural hearing loss is also evident at the level of the auditory midbrain.
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The structural changes associated with noise-induced temporary threshold shift (TTS) were compared to the damage associated with permanent threshold shift (PTS). A within-animal paradigm involving survival-fixation was used to minimize problems with data interpretation from interanimal variability in response to noise. Auditory brainstem response thresholds for clicks and tone pips were determined pre- and 1-2 h post-exposure in 11 chinchillas. ⋯ The other cochlea with PTS had buckled pillars in the corresponding frequency region. These results suggest that with moderate levels of noise exposure, buckling of the supporting cells results in an uncoupling of the OHC stereocilia from the tectorial membrane which results in a TTS. The mechanisms resulting in TTS appear to be distinct from those that produce permanent hair cell damage and a PTS.
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Carboplatin preferentially destroys inner hair cells (IHCs) in the chinchilla inner ear, while retaining a near-normal outer hair cell (OHC) population. The present study investigated the functional consequences of IHC loss on the compound action potential (CAP), inferior colliculus potential (ICP) and auditory cortex potential (ACP) recorded from chronically implanted electrodes. IHC loss led to a reduction in CAP amplitude that was roughly proportional to IHC loss. ⋯ In other animals, the ACP remained enhanced up to 5 weeks post-carboplatin. We interpret the transient and sustained enhancement of ACP amplitude following partial IHC loss as evidence of functional reorganization occurring at or below the level of the auditory cortex. These results suggest that the gain of the central auditory pathway increases following IHC loss to compensate for the reduced input from the cochlea.