Time course of organ of Corti degeneration after noise exposure.

From our permanent collection of plastic-embedded flat preparations of chinchilla cochleae, 22 controls and 199 ears from noise-exposed animals were used to determine when, postexposure, hair cell (HC) and supporting cell (SC) degeneration were completed. The exposed ears were divided into four groups based on exposure parameters: 0.5- or 4-kHz octave band of noise at moderate (M) or high (H) intensities.

Calibrated finger rub auditory screening test (CALFRAST).

Background: Determination of auditory function is a fundamental part of a complete neurologic examination. Disability from permanent hearing loss is common in the general population. Current bedside auditory tests are unreliable and cumbersome.

Relation of focal hair-cell lesions to noise-exposure parameters from a 4- or a 0.5-kHz octave band of noise.

In a previous study, we examined the relation between total energy in a noise exposure and the percentage losses of outer (OHC) and inner (IHC) hair cells in the basal and apical halves of 607 chinchilla cochleae [Harding, G.W., Bohne, B.

Effect of infrasound on cochlear damage from exposure to a 4 kHz octave band of noise.

Infrasound (i.e., <20 Hz for humans; <100 Hz for chinchillas) is not audible, but exposure to high-levels of infrasound will produce large movements of cochlear fluids.

Distribution of focal lesions in the chinchilla organ of Corti following exposure to a 4-kHz or a 0.5-kHz octave band of noise.

An octave band of noise (OBN) delivers fairly uniform acoustic energy over a specific range of frequencies. Above and below this range, energy is at least 30 dB SPL less than that within the OBN. When the ear is exposed to an OBN, hair-cell loss often occurs outside the octave band.

Death pathways in noise-damaged outer hair cells.

Using morphological criteria, death pathways in outer hair cells (OHCs) were determined in chinchilla organs of Corti that had been exposed to a high- or moderate-level octave band of noise (OBN) centered at either 0.5 or 4-kHz. The specimens were part of our large collection of plastic-embedded flat preparations of chinchilla cochleae.

The effect of an age-related hearing loss gene (Ahl) on noise-induced hearing loss and cochlear damage from low-frequency noise.

Inbred C57BL/6J mice carry two copies of an age-related hearing loss gene (Ahl). It has been shown that these mice begin losing high-frequency hearing at two months. Several functional studies have reported that the Ahl gene renders mice more susceptible to noise-induced hearing loss (NIHL) than strains which do not carry this gene [e.

Temporary DPOAE level shifts, ABR threshold shifts and histopathological damage following below-critical-level noise exposures.

DPOAE temporary level shift (TLS) at 2f(1)-f(2) and f(2)-f(1), ABR temporary threshold shift (TTS), and detailed histopathological findings were compared in three groups of chinchillas that were exposed for 24 h to an octave band of noise (OBN) centered at 4 kHz with a sound pressure level (SPL) of 80, 86 or 92 dB (n=3,4,6). DPOAE levels at 39 frequencies from f(1)=0.3 to 16 kHz (f(2)/f(1)=1.

The Digital Cytocochleogram.

The Mouse Cochlea Database (MCD) is a collection of resources that include digital images and bibliographic information on the mouse cochlea and is available at: http://mousecochlea.ccgb.umn.

Noise-induced hair-cell loss and total exposure energy: analysis of a large data set.

The relation between total noise-exposure energy, recovery time, or rest during the exposure and amount of hair-cell loss was examined in 416 chinchillas. The exposures were octave bands of noise (OBN) with a center frequency of either 4 kHz at 47-108 dB sound pressure level (SPL) for 0.5 h to 36 d, or 0.

An in vivo tracer study of noise-induced damage to the reticular lamina.

An in vivo tracer was used to determine if the reticular lamina and/or the cell membranes abutting the endolymphatic space are temporarily disrupted after intense noise exposure (4-kHz OBN, 108-dB SPL, 1.75 h). Using a double-barreled micropipette, the endolymphatic potential (EP) was recorded and artificial endolymph containing 10% carbon particles was injected into the endolymphatic space either 0 days or 28 days post-exposure.

DPOAE level shifts and ABR threshold shifts compared to detailed analysis of histopathological damage from noise.

A detailed comparison of 2f(1)-f(2) distortion product otoacoustic emission (DPOAE) level shifts (LS) and auditory brainstem response (ABR) threshold shifts with noise-induced histopathology was conducted in chinchillas. DPOAE levels (i.e.

Hereditary familial vestibular degenerative diseases.

Identification of genes involved in hereditary vestibular disease is growing at a remarkable pace. Mutant mouse technology can be an important tool for understanding the biological mechanism of human vestibular diseases.

Origin of vestibular dysfunction in Usher syndrome type 1B.

It is still debated to what extent the vestibular deficits in Usher patients are due to either central vestibulocerebellar or peripheral vestibular problems. Here, we determined the origin of the vestibular symptoms in Usher 1B patients by subjecting them to compensatory eye movement tests and by investigating the shaker-1 mouse model, which is known to have the same mutation in the myosin-VIIa gene as Usher 1B patients. We show that myosin-VIIa is not expressed in the human or mouse cerebellum and that the vestibulocerebellum of both Usher 1B patients and shaker-1 mice is functionally intact in that the gain and phase values of their optokinetic reflex are normal.

Degeneration in the cochlea after noise damage: primary versus secondary events.

Purpose: To determine if noise damage in the organ of Corti is different in the low- and high-frequency regions of the cochlea.

Materials And Methods: Chinchillas were exposed for 2 to 432 days to a 0.5 (low-frequency) or 4 kHz (high-frequency) octave band of noise at 47 to 95 dB sound pressure level.

An anatomically based frequency-place map for the mouse cochlea.

An anatomically based frequency-place map was created for the mouse using C57BL/CBA F1 hybrids by matching noise-induced lesions in the organ of Corti with permanent hearing losses as determined by auditory brainstem response (ABR) thresholds. Twenty-six mice developed 'notched' ABR threshold shifts after exposure to an octave band of noise with a center frequency of 2 kHz at 120 dB SPL for 24 h, 4 kHz at 110 dB SPL for 4 h or 8 kHz at 100 dB SPL for 1 or 2 h. ABR thresholds were determined at several intervals post-exposure until thresholds stabilized (14-27 days).

Noise damage in the C57BL/CBA mouse cochlea.

The present study was designed to determine the response to noise of the auditory system of a genetically well-defined laboratory mouse in preparation for examining the effect of noise on mice with specific genetic mutations. The mice were C57BL/CBA F1 hybrids. Eight mice served as non-noise-exposed controls and 39 mice were exposed for 1-24 h to an octave band of noise with a center frequency of 2, 4 or 8 kHz and a sound pressure level of 100-120 dB.

Histopathological differences between temporary and permanent threshold shift.

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.

Survival-fixation of the cochlea: a technique for following time-dependent degeneration and repair in noise-exposed chinchillas.

To minimize problems with data interpretation due to interanimal variation in susceptibility to noise, we developed a survival-fixation paradigm which involves fixing one cochlea of an experimental chinchilla at one post-exposure time and fixing the second cochlea as much as 14-24 days later. This paradigm is analytically effective because there is a high correlation in the magnitude and pattern of damage in the left and right cochleas of binaurally exposed animals. Thus, each experimental animal provides two snapshots in the degeneration and repair continua in which it can be certain that both cochleas sustained equivalent amounts of damage during the exposure.

High-resolution mapping of tlt, a mouse mutant lacking otoconia.

The ability to sense gravity is enhanced by an extracellular structure that overlies the macular sensory epithelium. This complex consists of high density particles, otoconia, embedded within a gelatinous membrane. The tilted mouse specifically lacks otoconia, yet has no other detectable anatomic lesions.

The role of micro-noise trauma in the etiology of aging-related changes in the inner ear.

Eleven chinchillas between 1 and 2.4 years of age had the malleus/incus complex removed from one middle ear and then lived in the Washington University animal facilities for 4 years post-surgery. Each animal had one ear (termed ambient-noise) in which the conductive apparatus was intact; the other ear (termed noise-protected) had a 50-60 dB conductive hearing loss.

Otoconial agenesis in tilted mutant mice.

The sense of balance is one of the phylogenetically oldest sensory systems. The vestibular organs, consisting of sensory hair cells and an overlying extracellular membrane, have been conserved throughout vertebrate evolution. To better understand mechanisms regulating vestibular development and mechanisms of vestibular pathophysiology, we have analyzed the mouse mutant, tilted (tlt), which has dysfunction of the gravity receptors.