Jaro-journal of The Association for Research in Otolaryngology 

About: Jaro-journal of The Association for Research in Otolaryngology is an academic journal published by Springer Science+Business Media. The journal publishes majorly in the area(s): Cochlea & Hair cell. It has an ISSN identifier of 1438-7573. Over the lifetime, 1066 publications have been published receiving 40761 citations. The journal is also known as: JARO (Print) & JARO (Internet).

Dynamics of noise-induced cellular injury and repair in the mouse cochlea.

Abstract: To assess the dynamics of noise-induced tissue injury and repair, groups of CBA/CaJ mice were exposed to an octave-band noise for 2 hours at levels of 94, 100, 106, 112, or 116 dB SPL and evaluated at survival times of 0, 12, 24 hours or 1, 2, or 8 weeks. Functional change, assessed via auditory brainstem response (ABR), ranged from a reversible threshold shift (at 94 dB) to a profound permanent loss (at 116 dB). Light microscopic histopathology was assessed in serial thick plastic sections and involved quantitative evaluation of most major cell types within the cochlear duct, including hair cells (and their stereocilia), supporting cells, ganglion cells, spiral ligament fibrocytes, spiral limbus fibrocytes, and the stria vascularis. Morphometry allowed patterns of damage to be systematically assessed as functions of (1) cochlear location, (2) exposure level, and (3) postexposure survival. Insights into mechanisms of acute and chronic noise-induced cellular damage are discussed.

Primary Neural Degeneration in the Guinea Pig Cochlea After Reversible Noise-Induced Threshold Shift

Abstract: Recent work in mouse showed that acoustic overexposure can produce a rapid and irreversible loss of cochlear nerve peripheral terminals on inner hair cells (IHCs) and a slow degeneration of spiral ganglion cells, despite full recovery of cochlear thresholds and no loss of inner or outer hair cells (Kujawa and Liberman, J Neurosci 29:14077–14085, 2009). This contrasts with earlier ultrastructural work in guinea pig suggesting that acute noise-induced neural degeneration is followed by full regeneration of cochlear nerve terminals in the IHC area (Puel et al., Neuroreport 9:2109–2114, 1998; Pujol and Puel, Ann N Y Acad Sci 884:249–254, 1999). Here, we show that the same patterns of primary neural degeneration reported for mouse are also seen in the noise-exposed guinea pig, when IHC synapses and cochlear nerve terminals are counted 1 week post-exposure in confocal images from immunostained whole mounts and that the same slow degeneration of spiral ganglion cells occurs despite no loss of IHCs and apparent recovery of cochlear thresholds. The data cast doubt on prior claims that there is significant neural regeneration and synaptogenesis in the adult cochlea and suggest that denervation of the inner hair cell is an important sequela of “reversible” noise-induced hearing loss, which likely applies to the human ear as well.

Neomycin-induced hair cell death and rapid regeneration in the lateral line of zebrafish (Danio rerio).

Abstract: Mechanoreceptive hair cells are extremely sensitive to aminoglycoside antibiotics, including neomycin. Hair cell survival was assessed in larval wild-type zebrafish lateral line neuromasts 4 h after initial exposure to a range of neomycin concentrations for 1 h. Each of the lateral line neuromasts was scored in live fish for the presence or absence of hair cells using the fluorescent vital dye DASPEI to selectively label hair cells. All neuromasts were devoid of DASPEI-labeled hair cells 4 h after 500 µM neomycin exposure. Vital DASPEI staining was proportional to the number of hair cells per neuromast identified in fixed larvae using immunocytochemistry for acetylated tubulin and phalloidin labeling. The time course of hair cell regeneration in the lateral line neuromasts was also analyzed following neomycin-induced damage. Regenerated hair cells were first observed using live DASPEI staining 12 and 24 h following neomycin treatment. The potential role of proliferation in regenerating hair cells was analyzed. A 1 h pulse-fix protocol using bromodeoxyuridine (BrdU) incorporation was used to identify S-phase cells in neuromasts. BrdU incorporation in neomycin-damaged neuromasts did not differ from control neuromasts 4 h after drug exposure but was dramatically upregulated after 12 h. The proliferative cells identified during a 1 h period at 12 h after neomycin treatment were able to give rise to new hair cells by 24–48 h after drug treatment. The results presented here provide a standardized preparation for studying and identifying genes that influence vertebrate hair cell death, survival, and regeneration following ototoxic insults.

The role of temporal fine structure processing in pitch perception, masking, and speech perception for normal-hearing and hearing-impaired people.

Abstract: Complex broadband sounds are decomposed by the auditory filters into a series of relatively narrowband signals, each of which can be considered as a slowly varying envelope (E) superimposed on a more rapid temporal fine structure (TFS). Both E and TFS information are represented in the timing of neural discharges, although TFS information as defined here depends on phase locking to individual cycles of the stimulus waveform. This paper reviews the role played by TFS in masking, pitch perception, and speech perception and concludes that cues derived from TFS play an important role for all three. TFS may be especially important for the ability to “listen in the dips” of fluctuating background sounds when detecting nonspeech and speech signals. Evidence is reviewed suggesting that cochlear hearing loss reduces the ability to use TFS cues. The perceptual consequences of this, and reasons why it may happen, are discussed.

Noise susceptibility of cochlear implant users: the role of spectral resolution and smearing.

Abstract: The latest-generation cochlear implant devices provide many deaf patients with good speech recognition in quiet listening conditions. However, speech recognition deteriorates rapidly as the level of background noise increases. Previous studies have shown that, for cochlear implant users, the absence of fine spectro-temporal cues may contribute to poorer performance in noise, especially when the noise is dynamic (e.g., competing speaker or modulated noise). Here we report on sentence recognition by cochlear implant users and by normal-hearing subjects listening to an acoustic simulation of a cochlear implant, in the presence of steady or square-wave modulated speech-shaped noise. Implant users were tested using their everyday, clinically assigned speech processors. In the acoustic simulation, normal-hearing listeners were tested for different degrees of spectral resolution (16, eight, or four channels) and spectral smearing (carrier filter slopes of −24 or −6 dB/octave). For modulated noise, normal-hearing listeners experienced significant release from masking when the original, unprocessed speech was presented (which preserved the spectro-temporal fine structure), while cochlear implant users experienced no release from masking. As the spectral resolution was reduced, normal-hearing listeners’ release from masking gradually diminished. Release from masking was further reduced as the degree of spectral smearing increased. Interestingly, the mean speech recognition thresholds of implant users were very close to those of normal-hearing subjects listening to four-channel spectrally smeared noise-band speech. Also, the best cochlear implant listeners performed like normal-hearing subjects listening to eight- to 16-channel spectrally smeared noise-band speech. These findings suggest that implant users’ susceptibility to noise may be caused by the reduced spectral resolution and the high degree of spectral smearing associated with channel interaction. Efforts to improve the effective number of spectral channels as well as reduce channel interactions may improve implant performance in noise, especially for temporally modulated noise.