Audiology & neuro-otology
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Audiology & neuro-otology · Mar 2001
Functional recovery of hearing following ampa-induced reversible disruption of hair cell afferent synapses in the avian inner ear.
Hair cells in the avian inner ear can regenerate after acoustic trauma or ototoxic insult, and significant functional recovery from hearing loss occurs. However, small residual deficits remain, possibly as a result of incomplete reestablishment of the hair cell neural synaptic contacts. The aim of the present study was to determine if intracochlear application of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), an excitotoxic glutamate agonist, causes reversible disruption of hair cell neural contacts in the bird, and to what extent functional recovery occurs if synaptic contacts are reestablished. ⋯ The process of neosynaptogenesis was completed 14 days after exposure. The present findings are strong evidence for a role of glutamate or a related excitatory amino acid as the afferent transmitter in the avian inner ear. In addition they show that functional recovery after disruption and regeneration of hair cell neural synapses, without apparent damage to the hair cells, is incomplete.
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Audiology & neuro-otology · Sep 2000
D-Methionine attenuates inner hair cell loss in carboplatin-treated chinchillas.
Carboplatin, a second-generation platinum-based antineoplastic drug, preferentially destroys inner hair cells (IHCs) in the chinchilla while sparing outer hair cells (OHCs). D-Methionine (D-Met), a sulfur-containing amino acid, has been shown to protect hair cells from cisplatin damage in rats, but its ability to protect IHCs from carboplatin damage has not yet been evaluated in the chinchilla. We tested whether D-Met would protect the hair cells in the chinchilla from carboplatin. ⋯ Ototoxicity was assessed by measuring the amount of IHC and OHC loss. Average IHC loss in the group treated with D-Met was 62% compared with 84% in the untreated control group. Thus, D-Met causes a statistically significant reduction in IHC loss induced by carboplatin.
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Mismatch negativity (MMN) and N100 auditory evoked potential were recorded in 52 healthy subjects and in 128 severely comatose patients. The MMN was present in 33/128 patients and N100 in 84/128. ⋯ The amplitudes of MMN and N100 in comatose patients were smaller than those of healthy subjects. It is concluded that MMN and N100 can be very useful in predicting whether or not a comatose patient will regain consciousness.
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Audiology & neuro-otology · Nov 1999
ReviewFunctional recovery in the avian ear after hair cell regeneration.
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 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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Audiology & neuro-otology · Nov 1999
ReviewStructural recovery from sound and aminoglycoside damage in the avian cochlea.
Hair cell regeneration in the mature avian cochlea occurs in response to trauma that causes the death of some or all of the existing hair cell population. In general, this trauma has been introduced experimentally by either sound overexposure or treatment of the bird with high doses of aminoglycoside antibiotics. When injured hair cells are ejected from the sensory epithelium, the nonsensory supporting cells respond by re-entering the cell cycle and proliferating or by transdifferentiating directly into hair cells without a mitotic event. ⋯ It will define how hair cells and nerve endings are lost and the tectorial membrane is damaged by the traumatizing stimuli and how the supporting cells and nerve fibers respond by producing new hair cells, a new tectorial membrane and new synaptic connections during recovery. Finally, it will focus on mechanisms that control the proliferation and transdifferentiation of supporting cells and the differentiation of new hair cells. This structural review is accompanied by a companion review that covers the fundamental issues concerning functional recovery in the avian cochlea associated with hair cell regeneration.