Developmental hearing loss impairs signal detection in noise: putative central mechanisms

Voytenko, S.V.; Galazyuk, Alexander V.; Rosen, Merri J.

doi:10.3389/fnsys.2014.00162

Cited by 27 publications

(22 citation statements)

References 90 publications

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“…To induce CHL in experimental animals, several approaches have been used. Beside plugging the auditory canal [14][15][16] or filling the middle ear cavity using poloxamer 22 , CHL was also induced by malleus removal 11,21,[39][40][41] as in the present study. In previous studies the effectivity of an experimental induced CHL was typically examined by measuring auditory brainstem responses (ABRs) which massively decreased to all delivered sound intensities and frequencies after this intervention 14,16 .…”

Section: Discussionsupporting

confidence: 49%

Homeostatic plasticity and synaptic scaling in the adult mouse auditory cortex

Teichert¹,

Liebmann

Hübner

et al. 2017

Sci Rep

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It has been demonstrated that sensory deprivation results in homeostatic adjustments recovering neuronal activity of the deprived cortex. For example, deprived vision multiplicatively scales up mEPSC amplitudes in the primary visual cortex, commonly referred to as synaptic scaling. However, whether synaptic scaling also occurs in auditory cortex after auditory deprivation remains elusive. Using periodic intrinsic optical imaging in adult mice, we show that conductive hearing loss (CHL), initially led to a reduction of primary auditory cortex (A1) responsiveness to sounds. However, this was followed by a complete recovery of A1 activity evoked sounds above the threshold for bone conduction, 3 days after CHL. Over the same time course patch-clamp experiments in slices revealed that mEPSC amplitudes in A1 layers 2/3 pyramids scaled up multiplicatively in CHL mice. No recovery of sensory evoked A1 activation was evident in TNFα KO animals, which lack synaptic scaling. Additionally, we could show that the suppressive effect of sounds on visually evoked visual cortex activity completely recovered along with TNFα dependent A1 homeostasis in WT animals. This is the first demonstration of homeostatic multiplicative synaptic scaling in the adult A1. These findings suggest that mild hearing loss massively affects auditory processing in adult A1.Homeostatic plasticity is essential in maintaining a stable firing rate in neurons to compensate for prolonged perturbations of neuronal activity 1,2 . For example, a prolonged reduction of neuronal activity of cultured neocortical neurons generated compensatory changes returning firing levels back to control values 1 . Such homeostatic regulations are typically accompanied by an additional insertion of 2-amino-3-(3-hydroxy-5-methyl-isoxasol-4-yl) propanoic acid receptors (AMPARs) into all synapses of a neuron, leading to multiplicatively scaled up mEPSC (miniature excitatory postsynaptic currents) amplitudes or, "synaptic scaling" 2,3 . Specifically, this mechanism is described to globally increase (or decrease) the strength of each synapse of a neuron by the same factor in a multiplicative manner which allows the conservation of information stored in the synaptic weights 4 . Previous studies have demonstrated that synaptic scaling also takes place in vivo, e.g. after reduction of sensory cortex activity due to sensory deprivation. For example, visual deprivation by intraocular TTX injections, dark exposure, binocular enucleation or retinal lesions scales up AMPAR mediated mEPSC amplitudes in layers 2/3 pyramids of the primary visual cortex (V1) in juvenile and adult mice [5][6][7][8][9] . Furthermore, it was shown that prolonged visual deprivation increases visually evoked V1 responses during the visual critical period 10 . However, evidence for homeostatic synaptic scaling in primary auditory cortex and its effects on cortical responsiveness following auditory deprivation is rare.Previously, two models for induction of an auditory deprivation have been used, sensorineural hearing...

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Section: Discussionsupporting

confidence: 49%

Homeostatic plasticity and synaptic scaling in the adult mouse auditory cortex

Teichert¹,

Liebmann

Hübner

et al. 2017

Sci Rep

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“…Smith and Zwislocki, 1975; Smith, 1979; Westerman and Smith, 1984), and is a nonlinearity that can only be explained by processes beyond the auditory nerve. Recent studies in animal models show cortical responses that are suggestive of overshoot (Gay et al 2014). Some previous studies (e.g.…”

Section: Discussionmentioning

confidence: 99%

Spatial and temporal disparity in signals and maskers affects signal detection in non-human primates

et al. 2017

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Detection thresholds for auditory stimuli (signals) increase in the presence of maskers. Natural environments contain maskers/distractors that can have a wide range of spatiotemporal properties relative to the signal. While these parameters have been well explored psychophysically in humans, they have not been well explored in animal models, and their neuronal underpinnings are not well understood. As a precursor to the neuronal measurements, we report the effects of systematically varying the spatial and temporal relationship between signals and noise in macaque monkeys (Macaca mulatta and Macaca radiata). Macaques detected tones masked by noise in a Go/No-Go task in which the spatiotemporal relationships between the tone and noise were systematically varied. Masked thresholds were higher when the masker was continuous or gated on and off simultaneously with the signal, and lower when the continuous masker was turned off during the signal. A burst of noise caused higher masked thresholds if it completely temporally overlapped with the signal, whereas partial overlap resulted in lower thresholds. Noise durations needed to be at least 100 ms before significant masking could be observed. Thresholds for short duration tones were significantly higher when the onsets of signal and masker coincided compared to when the signal was presented during the steady state portion of the noise (overshoot). When signal and masker were separated in space, masked signal detection thresholds decreased relative to when the masker and signal were co-located (spatial release from masking). Masking release was larger for azimuthal separations than for elevation separations. These results in macaques are similar to those observed in humans, suggesting that the specific spatiotemporal relationship between signal and masker determine threshold in natural environments for macaques in a manner similar to humans. These results form the basis for future investigations of neuronal correlates and mechanisms of masking.

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“…Another example of abnormal sound input early in life that could potentially lead to longer-term listening difficulties is temporary unilateral conductive loss due to infection of the middle ear, a condition named amblyaudia in analogy to the better known amblyopia ( Whitton & Polley 2011 ; Kaplan et al 2016 ). Animal studies have shown that short periods of such conductive loss can alter CANS development and disrupt binaural integration and hearing in noise even after a complete reversal of the loss ( Knudsen et al 1984 ; Popescu & Polley 2010 ; Polley et al 2013 ; Gay et al 2014 ). While some residual conductive loss sometimes remains in older children and adults with a history of middle ear infection, especially those who required multiple intubations (typically 5 to 10 dB, especially above 4 kHz; Hunter et al 1996 ), the bulk of the lingering difficulties hearing in noise is likely the result of impaired binaural hearing, as evidenced by poor performance on the masking level difference test ( Lynn et al 1981 ), for example ( Teele et al 1984 ; Pillsbury et al 1991 ; Wilmington et al 1994 ; Hall et al 1995 ; Hogan & Moore 2003 ; Gray et al 2009 ).…”

Section: Hidden Hearing Lossmentioning

confidence: 99%

On the Etiology of Listening Difficulties in Noise Despite Clinically Normal Audiograms

Pienkowski

2017

Ear &Amp; Hearing

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Many people with difficulties following conversations in noisy settings have “clinically normal” audiograms, that is, tone thresholds better than 20 dB HL from 0.1 to 8 kHz. This review summarizes the possible causes of such difficulties, and examines established as well as promising new psychoacoustic and electrophysiologic approaches to differentiate between them. Deficits at the level of the auditory periphery are possible even if thresholds remain around 0 dB HL, and become probable when they reach 10 to 20 dB HL. Extending the audiogram beyond 8 kHz can identify early signs of noise-induced trauma to the vulnerable basal turn of the cochlea, and might point to “hidden” losses at lower frequencies that could compromise speech reception in noise. Listening difficulties can also be a consequence of impaired central auditory processing, resulting from lesions affecting the auditory brainstem or cortex, or from abnormal patterns of sound input during developmental sensitive periods and even in adulthood. Such auditory processing disorders should be distinguished from (cognitive) linguistic deficits, and from problems with attention or working memory that may not be specific to the auditory modality. Improved diagnosis of the causes of listening difficulties in noise should lead to better treatment outcomes, by optimizing auditory training procedures to the specific deficits of individual patients, for example.

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Developmental hearing loss impairs signal detection in noise: putative central mechanisms

Cited by 27 publications

References 90 publications

Homeostatic plasticity and synaptic scaling in the adult mouse auditory cortex

Homeostatic plasticity and synaptic scaling in the adult mouse auditory cortex

Spatial and temporal disparity in signals and maskers affects signal detection in non-human primates

On the Etiology of Listening Difficulties in Noise Despite Clinically Normal Audiograms

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