Genetic dependence of cochlear cells and structures injured by noise

Ohlemiller, Kevin K.; Gagnon, Patricia M.

doi:10.1016/j.heares.2006.11.005

Cited by 57 publications

(84 citation statements)

References 79 publications

(109 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…6), in good agreement with previous studies in this and other mouse strains (Sadanaga and Morimitsu, 1995;Wu and Marcus, 2003;Ohlemiller and Gagnon, 2007b). There was no decline with age and EP remained high even in animals with severe elevations in ABR threshold.…”

Section: The Endocochlear Potential (Ep) Is Stable With Agingsupporting

confidence: 91%

Age-related auditory pathology in the CBA/J mouse

et al. 2008

View full text Add to dashboard Cite

Commercially obtained aged male CBA/J mice presented a complex pattern of hearing loss and morphological changes. A significant threshold shift in auditory brainstem responses (ABR) occurred at 3 months of age at 4 kHz without apparent loss of hair cells, rising slowly at later ages accompanied by loss of apical hair cells. A delayed high-frequency deficit started at 24 kHz around the age of 12 months. At 20 to 26 months, threshold shifts at 12 and 24 kHz and the accompanying hair cell loss at the base of the cochlea were highly variable with some animals appearing almost normal and others showing large deficits. Spiral ganglion cells degenerated by 18 months in all regions of the cochlea, with cell density reduced by approximately 25%. There was no degeneration of the stria vascularis and the endocochlear potential remained stable from 3 to 25 months of age regardless of whether the animals had normal or highly elevated ABR thresholds. The slow high frequency hearing loss combined with a modest reduction of ganglion cell density and an unchanged endocochlear potential suggest sensorineural presbycusis. The superimposed early hearing loss at low frequencies, which is not seen in animals bred in-house, may complicate the use of these animals as a presbycusis model.

show abstract

Section: The Endocochlear Potential (Ep) Is Stable With Agingsupporting

confidence: 91%

Age-related auditory pathology in the CBA/J mouse

et al. 2008

View full text Add to dashboard Cite

show abstract

“…The small increase in auditory thresholds as indicated by the ABR in the CBA/CaJ mice with age is in keeping with other studies, and this strain has been shown to maintain hearing well into advanced age [29]. There was a significant, albeit small, drop in the magnitude of EP in older mice, which has also been reported by Ohlemiller and Gagnon [30]. As EP provides a component of the driving force for hair cell transduction, EP magnitude and auditory threshold, as measured by sensitivity of individual spiral ganglion neurons, are intimately correlated [31].…”

Section: Discussionsupporting

confidence: 90%

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

Telang

Paramananthasivam

Vlajkovic

et al. 2010

Purinergic Signalling

View full text Add to dashboard Cite

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.

show abstract

“…S1) and demonstrated slightly smaller reductions in SEP magnitudes in response to trauma than did 40AG13, suggesting that genetic background differences affect hearing sensitivity and response to physiological perturbation. Genomic differences have significant effects on the susceptibility and response to interventions in NIHL and age-related hearing loss in mice (32,33) and humans (34). A strength of Drosophila is that rapid generation times, large number of lines, and diverse molecular and genomic tools enable large-scale and fine-resolution genetic studies, making it an excellent system to study interactions between genetic background effects and NIHL.…”

Section: Discussionmentioning

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.

View full text Add to dashboard Cite

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...

show abstract

Genetic dependence of cochlear cells and structures injured by noise

Cited by 57 publications

References 79 publications

Age-related auditory pathology in the CBA/J mouse

Age-related auditory pathology in the CBA/J mouse

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

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

Contact Info

Product

Resources

About