Hearing research
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The extent of hair cell regeneration following acoustic overstimulation severe enough to destroy tall hair cells, was determined in adult pigeons. BrdU (5-bromo-2'-deoxyuridine) was used as a proliferation marker. Recovery of hearing thresholds in each individual animal was measured over a period of up to 16 weeks after trauma. ⋯ In the area neural to this band, hair cells survive the overstimulation. In the area abneural to this band, sound damage is so severe, that no regeneration of hair cells occurs. As a consequence morphological and functional deficits persist.
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Comparative Study
Electrically evoked compound action potentials of guinea pig and cat: responses to monopolar, monophasic stimulation.
We recorded electrically evoked compound action potentials (EAPs) from guinea pigs and cats using monophasic current pulses delivered by a monopolar intracochlear electrode. By using simple stimuli, we sought results that could shed light on basic excitation properties of the auditory nerve. In these acute experiments, the recording electrode was placed directly on the auditory nerve. ⋯ In most cases where EAP saturation amplitude could be measured, that amplitude was similar for anodic and cathodic stimuli, suggesting that either stimulus polarity can recruit all fibers, or at least a comparable numbers of fibers. The common findings (e.g., EAP morphology and polarity-dependent latency) observed in these two species suggest results that can be extrapolated to responses obtained in humans, while the species-specific findings (e.g., dependence of threshold on polarity) may point to underlying anatomical differences that caution against overgeneralization across species. Some of our observations also bear upon hypotheses of how electrical stimuli may excite different sites on auditory nerve fibers.
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Chinchillas (n = 6) were treated with carboplatin and, following a 30-day recovery period, were exposed to a 115 dB peak SPL impact noise presented at a rate of l/s for 6 h/day for 10 days. A second group (n = 6) received only the noise treatment. Cubic distortion product otoacoustic emissions (2f1-f2) and auditory evoked potential (AEP) detection thresholds in response to tone bursts were measured before and 30 days after drug treatment and following the first and 10th day of the noise exposure. ⋯ AEP thresholds were elevated about 10 dB at the low frequencies in the drug-noise group whereas emissions returned to near normal despite the massive IHC losses. These results are consistent with the idea that an intact OHC population is required for toughening. However, sound-evoked efferent pathways activated by the few remaining IHCs (approximately 20%) which, in this preparation, are distributed throughout the cochlea, may still contribute significantly to the toughening phenomena.
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Comparative Study
Exposure to an augmented acoustic environment alters auditory function in hearing-impaired DBA/2J mice.
The effects of exposure to an augmented acoustic environment (AAE) on auditory function were evaluated using DBA/2J (DBA) mice, a strain that exhibits high-frequency hearing loss beginning around the time of weaning/adolescence (between 3-4 weeks of age) and becoming severe by 2-3 months of age. Mice were exposed 12 h per night for 10 nights to a 70 dB SPL broad-band noise AAE at one of three age periods ranging from the onset of hearing loss (25-35 days of age) to more severe degrees of hearing loss (35-45 days and 45-55 days); control mice did not receive the AAE. C57BL/6J (C57) mice of the same ages provided normal-hearing. age-matched mice in both exposed and control conditions. ⋯ The AAE had significant effects on DBA mice, but had no effect on normal-hearing C57 mice. For the most part, AAE exposure resulted in improved auditory performance in DBA mice (better PPI, lower ABR thresholds, bigger startle amplitudes). However, the age of the mice and/or severity of hearing loss proved to be an important variable; improvement of PPI occurred only when the AAE was initiated later in the course of hearing loss (35 days of age or older); in contrast to this, beneficial effects on ABR thresholds occurred only when the AAE was initiated early in the course of hearing loss (< 45 days of age).
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In the cochlea, outer hair cells (OHCs) generate the active cochlear mechanics whereas the supporting cells, such as Deiters' cells and Hensen's cells, may play a role in both the active and passive cochlear mechanics. The presence of receptors for adenosine triphosphate (ATP) on OHCs, Deiters' cells and Hensen's cells indicates that endogenous ATP may have a role in cochlear mechanics. To explore this possibility, the effects of the ATP antagonist, pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS), were studied in guinea pig both in vitro on isolated OHCs, Deiters' cells, Hensen's cells and pillar cells using the whole-cell configuration of the patch-clamp technique, and in vivo on sound evoked cochlear potentials (cochlear microphonic, CM; summating potential, SP; compound action potential, CAP) and distortion product otoacoustic emissions (DPOAEs) using cochlear perilymphatic perfusion. ⋯ In vivo application of PPADS in increasing concentrations reduced the sound evoked CAP, SP and increased N1 latency starting at about 0.33 mM (SP) and 1 mM (CAP and N1 latency). PPADS (0.33-1 mM) reversibly suppressed the initial value of the quadratic DPOAE and reversed the 'slow decline' in the quadratic DPOAE that occurs during continuous stimulation with moderate level primaries. These results, together with the similar effects of the ATP antagonist suramin reported previously (Skellett et al., 1997), may be evidence that endogenous ATP acting on cells in the organ of Corti alters cochlear mechanics.