The influence of noise exposure on the parameters of a convolution model of the compound action potential

Chertoff, Mark E.; Lichtenhan, Jeffery T.; Tourtillott, B. M.; Esau, K. S.

doi:10.1121/1.2967890

Cited by 8 publications

(11 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Latency reductions are probably due to the particular mammalian cochlea mechanical tonotopy and tuning properties. Increasing probe SPLs to elicit a response in a tonotopic region with trauma-induced threshold shift may activate fibers with a much higher center frequency, which are more basal in the cochlea and have a smaller traveling wave delay and shorter latency (11,36). Basilar membrane mechanical property changes from OHC damage are also implicated in latency reduction (35,36).…”

Section: Discussionmentioning

confidence: 99%

“…It is currently thought that reduced CAP after intense sound trauma is caused by reduced AN fiber recruitment (resulting from damage or death of hair cells and/or spiral ganglion neurons) and from a "broadening" of the response from desynchronization of afferents with similar center frequencies (11,36). Also, hair cells or AN fiber death or degeneration may occur over days to months (6,9).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

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

Section: Discussionmentioning

confidence: 99%

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

show abstract

“…Figure 1A presents an example of the high correlations achieved by Chertoff (2004) and in the current study between the analytic CAPs (gray line) and actual CAPs elicited from normal ears (black line). Chertoff et al (2008) showed that the analytic CAP could also reliably model CAPs recorded from animals after noise exposure. Lichtenhan and Chertoff (2008) extended the use of the convolution model to CAPs recorded with a custom tympanic membrane electrode (Ferraro & Durrant 2002) from human subjects with temporary noise-induced hearing threshold shifts.…”

Section: Introductionmentioning

confidence: 98%

“…Mills (2006) suggested that the combined use of auditory brain stem response (ABR) thresholds and distortion-product otoacoustic emission (DPOAE) amplitudes could differentiate between hearing loss related to stria vascularis damage and noise-induced hearing loss in an animal model. Chertoff (2004), Chertoff et al (2008), and Lichtenhan and Chertoff (2008) investigated the utility of the compound action potential (CAP) in identifying auditory nerve fiber degeneration associated with sensorineural hearing loss. Their approach was to characterize CAP morphology using Goldstein and Kiang's (1958) mathematical model given as,…”

Section: Introductionmentioning

confidence: 99%

Predicting Auditory Nerve Survival Using the Compound Action Potential

Earl

Chertoff

2010

Ear &Amp; Hearing

View full text Add to dashboard Cite

Consistent with previous findings, physiological measures of threshold were not correlated with partial lesions of the auditory nerve. The model parameter N at high-stimulus levels was strongly correlated with normal nerve area suggesting, that it is a good predictor of auditory nerve survival. The model parameter N also seemed to be a better predictor of the condition of the auditory nerve than the conventional measure of N1 amplitude. Because the model parameter f was correlated with normal nerve area at low- and high-stimulus levels, it may provide information on the functional status of the auditory nerve.

show abstract

“…Other studies in the cochlear implant literature have indicated that the amplitude of electrically evoked auditory potentials is positively correlated with the number of viable auditory neurons (Smith and Simmons, 1983;Hall, 1990) and may gauge prognoses for implant recipients (Gibson and Sanli, 2007;Teagle et al, 2010). Chertoff (2004) and Chertoff et al (2008) used a gerbil model to determine the utility of the compound action potential (CAP) for quantifying auditory nerve pathology. Their approach was to analyze the morphology of CAPs by fitting the waveforms with a five-parameter convolution model adapted from Goldstein and Kiang's (1958) description of the CAP as the sum of synchronously firing auditory neurons.…”

Section: Introductionmentioning

confidence: 99%

Mapping auditory nerve firing density using high-level compound action potentials and high-pass noise masking

Earl

Chertoff

2012

The Journal of the Acoustical Society of America

View full text Add to dashboard Cite

Future implementation of regenerative treatments for sensorineural hearing loss may be hindered by the lack of diagnostic tools that specify the target(s) within the cochlea and auditory nerve for delivery of therapeutic agents. Recent research has indicated that the amplitude of high-level compound action potentials (CAPs) is a good predictor of overall auditory nerve survival, but does not pinpoint the location of neural damage. A location-specific estimate of nerve pathology may be possible by using a masking paradigm and high-level CAPs to map auditory nerve firing density throughout the cochlea. This initial study in gerbil utilized a high-pass masking paradigm to determine normative ranges for CAP-derived neural firing density functions using broadband chirp stimuli and low-frequency tonebursts, and to determine if cochlear outer hair cell (OHC) pathology alters the distribution of neural firing in the cochlea. Neural firing distributions for moderateintensity (60 dB pSPL) chirps were affected by OHC pathology whereas those derived with high-level (90 dB pSPL) chirps were not. These results suggest that CAP-derived neural firing distributions for high-level chirps may provide an estimate of auditory nerve survival that is independent of OHC pathology.

show abstract

The influence of noise exposure on the parameters of a convolution model of the compound action potential

Cited by 8 publications

References 27 publications

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

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

Predicting Auditory Nerve Survival Using the Compound Action Potential

Mapping auditory nerve firing density using high-level compound action potentials and high-pass noise masking

Contact Info

Product

Resources

About