Recent findings and emerging questions in cochlear noise injury

Ohlemiller, Kevin K.

doi:10.1016/j.heares.2008.08.007

Cited by 75 publications

(58 citation statements)

References 179 publications

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“…In vertebrates, acoustic trauma often correlates with stereocilia disruption (37), OHC and IHC damage or loss (4,6,7,26,37), spiral ganglion cell loss (6,7,14,37), and damage to supporting tissue and nonsensory cochlear cell types (6,7). Although nompC is an important mechanosensitive channel in Drosophila auditory function (18,38,39), the identity, arrangement and structure of other mechanotransduction system elements (e.g., additional mechanosensitive ion channels, support and connector proteins) in JO sensory neuron cilia are unclear (40).…”

Section: Discussionmentioning

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).…”

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confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

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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“…Within the cochlea, aminoglycosides preferentially injure the stria vascularis and outer hair cells (Taylor et al 2008;Rizzi and Hirose 2007;Forge and Schacht 2000). Although noise can also injure the stria, the injury appears largely reversible under all but the most extreme conditions Hirose and Liberman 2003), and it is not clear that lateral wall events can ultimately impact the extent of NIPTS (Ohlemiller 2008). Since OHC function and survival represent the most salient common target of both noise and KM, we suggest that preservation of OHC function and survival constitutes the most likely locus of KM-related protective mechanisms and that KM engages protective cascades within OHCs.…”

Section: Cells Impacted By Noise and Protected By Kmmentioning

confidence: 99%

Protection against Noise-Induced Hearing Loss in Young CBA/J Mice by Low-Dose Kanamycin

Fernandez

Ohlemiller

Gagnon

et al. 2010

JARO

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Animal studies indicate that a combination of kanamycin (KM) and noise produces a synergistic effect, whereby the threshold shift from the combination is greater than the sum of the shifts caused by either agent alone. Most such studies have focused on adult animals, and it has remained unclear whether younger, presumably more susceptible, animals show an even greater synergistic effect. The present study tested the hypothesis that young CBA/J mice receiving a low dose of KM (300 mg/kg, 2×/day, s.c.) from 20 to 30 days post-gestational age followed by brief noise exposure (110 dB SPL; 4-45 kHz, 30 s) would show greater noise-induced permanent threshold shifts (NIPTS) than mice receiving either treatment alone. Noise exposure produced 30-40 dB of NIPTS and moderate hair cell loss in young saline-treated mice. KM alone at this dose had no effect on thresholds. Surprisingly, mice receiving KM plus noise were protected from NIPTS, showing ABR thresholds not significantly different from unexposed controls. Mice receiving KM prior to noise exposure also showed significantly less outer hair cell loss than saline-treated mice. Additional experiments indicated protection by KM when the noise was applied either 24 or 48 h after the last KM injection. Our results demonstrate a powerful protective effect of subchronic low-dose kanamycin against NIPTS in young CBA/J mice. Repeated kanamycin exposure may establish a preconditioned protective state, the molecular bases of which remain to be determined.

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“…Recently, Ohlemiller [46] reported that the effect of noise on EP in the mouse is strain-specific, which could indicate that the effect of noise on the EP generating mechanism may well be more variable and strain-specific than had been first thought. Notably, all animal models presently known to undergo an age-associated reduction in EP feature an environmental or stochastic component such that at most, half of the subjects exhibit an abnormally low EP at advanced ages.…”

Section: Discussionmentioning

confidence: 99%

Reduced P2x2 receptor-mediated regulation of endocochlear potential in the ageing mouse cochlea

Telang

Paramananthasivam

Vlajkovic

et al. 2010

Purinergic Signalling

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Extracellular adenosine triphosphate (ATP) has profound effects on the cochlea, including an effect on the regulation of the endocochlear potential (EP). Noise-induced release of ATP into the endolymph activates a shunt conductance mediated by P2X 2 receptors in tissues lining the endolymphatic compartment, which reduces the EP and, consequentially, hearing sensitivity. This may be a mechanism of adaptation or protection from high sound levels. As inaction of such a process could contribute to hearing loss, this study examined whether the action of ATP on EP changes with age and noise exposure in the mouse. The EP and the endolymphatic compartment resistance (CoPR) were measured in mice (CBA/CaJ) aged between 3 and 15 months. The EP and CoPR declined slightly with age with an associated small, but significant, reduction in auditory brainstem response thresholds. ATP (100-1,000 μM) microinjected into the endolymphatic compartment caused a dosedependent decline in EP correlated to a similar decrease in CoPR. This was blocked by pyridoxal-phosphate-6-azophenyl-2′,4′-disulfonate, consistent with a P2X 2 receptormediated shunt conductance. There was no substantial difference in the ATP response with age. Noise exposure (octave-band noise 80-100 decibels sound pressure level (dBSPL), 48 h) in young animals induced an upregulation of the P2X 2 receptor expression in the organ of Corti and spiral limbus, most noticeably with the 90-dB exposure. This did not occur in the aged animals except following exposure at 90 dBSPL. The EP response to ATP was muted in the noiseexposed aged animals except following the 90-dB exposure. These findings provide some evidence that the adaptive response of the cochlea to noise may be reduced in older animals, and it is speculated that this could increase their susceptibility to noise-induced injury.

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Recent findings and emerging questions in cochlear noise injury

Cited by 75 publications

References 179 publications

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

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

Protection against Noise-Induced Hearing Loss in Young CBA/J Mice by Low-Dose Kanamycin

Reduced P2x2 receptor-mediated regulation of endocochlear potential in the ageing mouse cochlea

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