Threshold Shift, Hair Cell Loss, and Hair Bundle Stiffness Following Exposure to 120 and 125 dB Pure Tones in the Neonatal Chick

Adler, Henry J.; Kenealy, J. F. X.; Dedio, Robert M.; Saunders, James C.

doi:10.3109/00016489209137425

Cited by 37 publications

(24 citation statements)

References 19 publications

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“…Its longitudinal location is independent of stimulus frequency [Rebillard et al, 1982;Ryals and Rubel, 1985a]. The extent of the damaged area and the area of hair cell loss increase towards the neural edge of the papilla and spread both apically and basally with increasing exposure intensity [Cotanche et al, 1987;Adler et al, 1992;Cotanche et al, 1995;Müller et al, 1996] and duration Ryals and Rubel, 1985a;Cotanche and Dopyera, 1990]. However, at the same stimulus level, damage does not increase with exposure duration beyond 48 h of exposure [Cotanche and Dopyera, 1990;Raphael, 1991;Pugliano et al, 1993b].…”

Section: Traumamentioning

confidence: 95%

Functional Recovery in the Avian Ear after Hair Cell Regeneration

Smolders

1999

Audiol Neurotol

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Trauma to the inner ear in birds, due to acoustic overstimulation or ototoxic aminoglycosides, can lead to hair cell loss which is followed by regeneration of new hair cells. These processes are paralleled by hearing loss followed by significant functional recovery. After acoustic trauma, functional recovery is rapid and nearly complete. The early and major part of functional recovery after sound trauma occurs before regenerated hair cells become functional. Even very intense sound trauma causes loss of only a proportion of the hair cell popu- lation, mainly so-called short hair cells residing on the abneural mobile part of the avian basilar membrane. Uncoupling of the tectorial membrane from the hair cells during sound overexposure may serve as a protection mechanism. The rapid functional recovery after sound trauma appears not to be associated with regeneration of the lost hair cells, but with repair processes involving the surviving hair cells. Small residual functional deficits after recovery are most likely associated with the missing upper fibrous layer of the tectorial membrane which fails to regenerate after sound trauma. After aminoglycoside trauma, functional recovery is slower and parallels the structural regeneration more closely. Aminoglycosides cause damage to both types of hair cells, starting at the basal (high frequency) part of the basilar papilla. However, functional hearing loss and recovery also occur at lower frequencies, associated with areas of the papilla where hair cells survive. Functional recovery in these low frequency areas is complete, whereas functional recovery in high frequency areas with complete hair cell loss is incomplete, despite regeneration of the hair cells. Permanent residual functional deficits remain. This indicates that in low frequency regions functional recovery after aminoglycosides involves repair of nonlethal injury to hair cells and/or hair cell-neural synapses. In the high frequency regions functional recovery involves regenerated hair cells. The permanent functional deficits after the regeneration process in these areas are most likely associated with functional deficits in the regenerated hair cells or shortcomings in the synaptic reconnections of nerve fibers with the regenerated hair cells. In conclusion, the avian inner ear appears to be much more resistant to trauma than the mammalian ear and possesses a considerable capacity for functional recovery based on repair processes along with its capacity to regenerate hair cells. The functional recovery in areas with regenerated hair cells is considerable but incomplete.

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Section: Traumamentioning

confidence: 95%

Functional Recovery in the Avian Ear after Hair Cell Regeneration

Smolders

1999

Audiol Neurotol

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“…2A) (Cotanche et al 1987;Henry et al 1988;Marsh et al 1990). Hair cells are lost from the basilar papilla in a pattern that is determined by the intensity of the pure-tone stimulus for a constant exposure time (Cotanche et al 1987;Adler et al 1992) or by the length of the exposure at a constant intensity (Cotanche and Dopyera 1990). For a constant exposure time (i.e., 48 h), the number of hair cells lost and the size of the noise-damaged region increases as the intensity of the exposure increases from 110 dB SPL to 125 dB SPL.…”

Section: Progression Of Noise Damage In the Basilar Papillamentioning

confidence: 99%

“…120 dB SPL), the number of hair cells lost and the size of the noise-damaged region increases as the length of the exposure is extended from 4 to 48 h. There seems to be some asymptotic level of damage when the intensity is held at 120 dB SPL, since exposures of up to 200 h have shown a region of damage similar to that seen at 48 h (Pugliano et al 1993b). In contrast, when intensities of 125 dB SPL or greater are used for exposures of at least 24 h, there can be an extensive spread in the severity and location of the damage that results in a complete destruction of the sensory epithelium over the basilar membrane (Cotanche et al 1987;Adler et al 1992). SEM studies have documented the progression of damage that results from increasing the length of puretone exposures (Anderson et al 1989;Cotanche and Dopyera 1990).…”

Section: Progression Of Noise Damage In the Basilar Papillamentioning

confidence: 99%

“…2C, D) (Cotanche 1987b;Marsh et al 1990). It has been estimated that up to 35% of the hair cells within the damaged region are lost after a 48-h exposure to a 120 dB SPL stimulus and up to 59% lost after a 125 dB SPL stimulus (Henry et al 1988;Marsh et al 1990;Adler et al 1992). The apical surfaces of the supporting cells within the damaged region expand to fill in areas around the contracting hair cell surfaces and in areas where hair cells have been lost (Fig.…”

Section: Progression Of Noise Damage In the Basilar Papillamentioning

confidence: 99%

“…Similarly, the extent of recovery and the number of new hair cells produced is also correlated with the length of the noise exposure. Short stimuli produce only a few new hair cells and a rapid recovery of the mosaic, while longer exposures lead to a larger number of new hair cells and a less complete repair of the basilar papilla (Marsh et al 1990;Adler et al 1992;Stone and Cotanche 1992). Surprisingly, though, there must be some point where asymptotic levels of noise damage occur in the cochlea, i.e.…”

Section: Recovery From Noise Damage In the Basilar Papillamentioning

confidence: 99%

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Hair cell regeneration in the bird cochlea following noise damage or ototoxic drug damage

et al. 1994

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Hair cells are sensory cells that transduce motion into neural signals. In the cochlea, they are used to detect sound waves in the environment and turn them into auditory signals that can be processed in the brain. Hair cells in the cochlea of birds and mammals were thought to be produced only during embryogenesis and, once made, they were expected to last throughout the lifetime of the animal. Thus, any loss of hair cells due to trauma or disease was thought to lead to permanent impairment of auditory function. Recently, however, studies from a number of laboratories have shown that hair cells in the avian cochlea can be regenerated after acoustic trauma or ototoxic drug damage. This regeneration is accompanied by a repair of the sensory organ and associated tissues and results in a recovery of auditory function. In this review, we examine and compare the structural events that lead to hair cell loss after noise damage and ototoxic drug damage as well as the processes involved in the recovery of the epithelium and the regeneration of the hair cells. Moreover, we examine functional recovery and how it relates to the structural recovery. Finally, we investigate the evidence for the hypothesis that supporting cells in the basilar papilla act as the progenitor cells for the regenerated hair cells and examine the cellular events required to stimulate the progenitor cells to leave the quiescent state, re-enter the cell cycle, and divide.

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Distribution of nerve fibers in the basilar papilla of normal and sound-damaged chick cochleae

Ofsie

Cotanche

1996

J. Comp. Neurol.

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Epifluorescent light microscopy and confocal laser scanning microscopy were employed to visualize the distribution of nerve fibers in whole-mount preparations of normal and sound-damaged chick basilar papillae (BP). In normal cochleae, we identified a consistent pattern of nerve processes that ran transversely across the BP. The transverse processes increase in number from the proximal to the distal ends of the epithelium. However, when the processes are separated into populations of thin fibers and thick bundles, the thin fibers are more prevalent in distal regions whereas thick bundles are more extensive in proximal regions. Furthermore, the thick bundles form an elaborate longitudinal network in the border cell and hyaline cell region. Based on these data and no other previous studies, the thin fibers appear to be afferent nerves and the thick bundles represent efferent nerves. When birds are exposed to acoustic trauma, the normal pattern and number of nerve processes is not altered by levels of sound that produce moderate levels of damage, i.e., damage that leads to hair cell loss and regeneration. However, the nerve pattern is disrupted by severe levels of damage that destroy both hair cells and supporting cells. These findings indicate that the level of sound exposure that induces hair cell regeneration may damage the synaptic endings associated with the lost hair cells, but that the nerve processes that give rise to these endings remain intact within the sensory epithelium. In contrast, severe damage destroys both the hair cells and their associated nerve fibers.

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Threshold Shift, Hair Cell Loss, and Hair Bundle Stiffness Following Exposure to 120 and 125 dB Pure Tones in the Neonatal Chick

Cited by 37 publications

References 19 publications

Functional Recovery in the Avian Ear after Hair Cell Regeneration

Functional Recovery in the Avian Ear after Hair Cell Regeneration

Hair cell regeneration in the bird cochlea following noise damage or ototoxic drug damage

Distribution of nerve fibers in the basilar papilla of normal and sound-damaged chick cochleae

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