Involvement of apoptosis in progression of cochlear lesion following exposure to intense noise

Hu, Bo; Henderson, Donald; Nicotera, Thomas M.

doi:10.1016/s0378-5955(02)00286-1

Cited by 214 publications

(181 citation statements)

References 27 publications

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“…Acoustic trauma is also known to induce hair cell and neuron death through formation of reactive oxygen species and free radicals (Duan et al, 2000;Lefebvre et al, 2002). It has been suggested that necrosis and apoptosis are simultaneously involved in hair cell death (Hu et al, 2002). The resulting hair cell death and lesions are assumed to be permanent in mammals (Duan et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Enriched Acoustic Environment after Noise Trauma Reduces Hearing Loss and Prevents Cortical Map Reorganization

Noreña¹,

Eggermont²

2005

J. Neurosci.

297

188

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Exposure to sound of sufficient duration and level causes permanent damage to the peripheral auditory system, which results in the reorganization of the cortical tonotopic map. The changes are such that neurons with pre-exposure tuning to frequencies in the hearing loss range now become tuned to frequencies near the near-normal lower boundary of the hearing loss range, which thus becomes over represented. However, cats exposed to a traumatizing noise and immediately thereafter placed for a few weeks in an enriched acoustic environment presented a much-restricted hearing loss compared with similarly exposed cats that were placed for the same time in a quiet environment. The enriched environment spectrally matched the expected hearing loss range and was ϳ40 dB above the level of the expected hearing loss. The hearing loss in the quiet environment-reared cats ranged from 6 to 32 kHz with the largest loss (on average, 40 dB) ranging from 24 to 32 kHz. In contrast, the hearing loss in the enriched-environment cats was restricted to 6 -8 kHz at a level of, on average, 35 dB and with 16 -32 kHz having normal thresholds. Despite the remaining hearing loss for the enriched-environment cats in the 6 -8 kHz range, plastic tonotopic map changes in primary auditory cortex could no longer be demonstrated, suggesting that the enriched acoustic environment prevents this reorganization. This finding has implications for the treatment of hearing disorders, such as tinnitus, that have been linked to cortical tonotopic map reorganization.

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Section: Discussionmentioning

confidence: 99%

Enriched Acoustic Environment after Noise Trauma Reduces Hearing Loss and Prevents Cortical Map Reorganization

Noreña¹,

Eggermont²

2005

J. Neurosci.

297

188

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“…In mammals, acoustic trauma induces metabolic stress in cochlear hair cells and spiral ganglion neurons, changing mitochondrial fission/fusion dynamics; with sufficiently intense trauma, this induces apoptosis pathways (5,26,27). To test whether flies with slightly compromised physiological components would be sensitized to acoustic trauma, we exposed flies heterozygous for a mutation in the nrv3 gene, encoding a Na + /K + ATPase β subunit specifically expressed in auditory neurons (23; Fig.…”

Section: Physiological/behavioral Responses To Trauma In Control Stramentioning

confidence: 99%

“…Importantly, intense acoustic trauma can induce permanent damage-unlike other vertebrates, mammals cannot regenerate auditory hair cells (1,2). NIHL associated with permanent changes in auditory sensitivity causes multiple consistent effects: stereocilia bundle disruption, inner (IHC) and outer hair cell (OHC) death or damage, supporting cell tissue disruption, and eventual spiral ganglion cell damage or loss (3)(4)(5)(6)(7). Most studies to date used mammalian model organisms such as mice (8,9), rats (10), and guinea pigs (11)(12)(13)(14).…”

mentioning

confidence: 99%

Physiological, anatomical, and behavioral changes after acoustic trauma in Drosophila melanogaster

Christie

Sivan-Loukianova

Smith

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Noise-induced hearing loss (NIHL) is a growing health issue, with costly treatment and lost quality of life. Here we establish Drosophila melanogaster as an inexpensive, flexible, and powerful genetic model system for NIHL. We exposed flies to acoustic trauma and quantified physiological and anatomical effects. Trauma significantly reduced sound-evoked potential (SEP) amplitudes and increased SEP latencies in control genotypes. SEP amplitude but not latency effects recovered after 7 d. Although trauma produced no gross morphological changes in the auditory organ (Johnston's organ), mitochondrial cross-sectional area was reduced 7 d after exposure. In nervana 3 heterozygous flies, which slightly compromise ion homeostasis, trauma had exaggerated effects on SEP amplitude and mitochondrial morphology, suggesting a key role for ion homeostasis in resistance to acoustic trauma. Thus, Drosophila exhibit acoustic trauma effects resembling those found in vertebrates, including inducing metabolic stress in sensory cells. This report of noise trauma in Drosophila is a foundation for studying molecular and genetic sequelae of NIHL. mitochondria | Na/K ATPase | locomotion | auditory courtship behavior N oise-induced hearing loss (NIHL) is a pervasive and growing health issue arising from occupational and recreational hazards, with significant costs in health care and personal quality of life. Despite this, the molecular and physiological mechanisms involved in the etiology or recovery from injury are not yet fully understood. Importantly, intense acoustic trauma can induce permanent damage-unlike other vertebrates, mammals cannot regenerate auditory hair cells (1, 2). NIHL associated with permanent changes in auditory sensitivity causes multiple consistent effects: stereocilia bundle disruption, inner (IHC) and outer hair cell (OHC) death or damage, supporting cell tissue disruption, and eventual spiral ganglion cell damage or loss (3-7). Most studies to date used mammalian model organisms such as mice (8, 9), rats (10), and guinea pigs (11)(12)(13)(14). These animals have difficult access to the inner ear inside the temporal bone and high maintenance costs coupled with relatively long generation times.Drosophila is a compelling alternative model system with strong genetic tools, inexpensive production of large numbers of animals, and an accessible auditory system that is becoming better understood genetically and physiologically. During courtship, Drosophila males vibrate their wings to produce a courtship song composed of pulse and sinusoidal components (15,16). This song facilitates species identification and mate selection (16,17). Drosophila males and females detect airborne vibrations via Johnston's organ (JO) in the second antennal segment (18). The JO is an array of chordotonal mechanoreceptors (or scolopidia; Fig. 1 A-C). Via the aristae, acoustic energy is transformed to rotational movement of the third antennal segment, activating mechanosensitive channels on JO neuron dendrites. Like vertebrate hair cells, JO ne...

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“…[12][13][14][15] Nevertheless, apoptosis is thought to have a significant role in noise-induced damage of the cochlea. 14,16,17 Apoptosis may be executed by a family of cysteine proteases called caspases. [18][19][20] To date, 14 caspases have been identified that are broadly divided into two groups, initiator (caspase-6, -8, -9 and -10) and executioner (caspase-2, -3 and -7).…”

Section: Introductionmentioning

confidence: 99%

“…18,21,22 In NIHL, apoptosis resulting from activation of the extrinsic pathway (caspase-8) or the intrinsic pathway (caspase-9) has been observed. 12,13,15,16 These two pathways converge on caspase-3, the final executioner of apoptosis. Both the intrinsic and extrinsic pathways are opposed by members of the inhibitor of apoptosis protein (IAPs) family.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of X-linked inhibitor of apoptosis protein protects against noise-induced hearing loss in mice

et al. 2011

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Apoptosis is responsible for cochlear cell death induced by noise. Here, we show that transgenic (TG) mice that overexpress X-linked inhibitor of apoptosis protein (XIAP) under control of the ubiquitin promoter display reduced hearing loss and cochlear damage induced by acoustic overstimulation (125 dB sound pressure level, 6 h) compared with wild-type (WT) littermates. Hearing status was evaluated using the auditory brainstem response (ABR), whereas cochlear damage was assessed by counts of surviving hair cells (HCs) and spiral ganglion neurons (SGNs) as well as their fibers to HCs. Significantly smaller threshold shifts were found for TG mice than WT littermates. Correspondingly, the TG mice also showed a reduced loss of HCs, SGNs and their fibers to HCs. HC loss was limited to the basal end of the cochlea that detects high frequency sound. In contrast, the ABRs demonstrated a loss of hearing sensitivity across the entire frequency range tested (2-32 kHz) indicating that the hearing loss could not be fully attributed to HC loss alone. The TG mice displayed superior hearing sensitivity over this whole range, suggesting that XIAP overexpression reduces noise-induced hearing loss not only by protecting HCs but also other components of the cochlea.

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Involvement of apoptosis in progression of cochlear lesion following exposure to intense noise

Cited by 214 publications

References 27 publications

Enriched Acoustic Environment after Noise Trauma Reduces Hearing Loss and Prevents Cortical Map Reorganization

Enriched Acoustic Environment after Noise Trauma Reduces Hearing Loss and Prevents Cortical Map Reorganization

Physiological, anatomical, and behavioral changes after acoustic trauma in Drosophila melanogaster

Overexpression of X-linked inhibitor of apoptosis protein protects against noise-induced hearing loss in mice

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