Age-related changes in event related potentials, steady state responses and temporal processing in the auditory cortex of mice with severe or mild hearing loss

Rumschlag, Jeffrey A.; Razak, Khaleel A.

doi:10.1016/j.heares.2021.108380

Cited by 14 publications

(20 citation statements)

References 81 publications

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“…If this contributes to hidden hearing loss, we here have encountered a well-known phenomenon which has historically been termed recruitment (Denes and Naunton, 1950) and is known to correlate to DPOAE I/O functions (Rasetshwane et al, 2013). As found in previous studies (Boettcher et al, 2001; Rumschlag and Razak, 2021) ASSR amplitude declined with age, although only showing a statistical tendency. We observed a higher ASSR amplitude in poor PNOT in ipsi-noise (Fig 8C) explaining 7% of the variance of speech-in-noise comprehension in the OLSA-BB condition, corresponding to 0.4 dB in SRT (Tab.…”

Section: Discussionsupporting

confidence: 84%

Neural adaptation at stimulus onset and speed of neural processing as critical contributors to speech comprehension independent of hearing threshold or age

Schirmer,

Wolpert,

Dapper

et al. 2023

Preprint

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Loss of afferent auditory fiber function (cochlear synaptopathy) has been suggested to occur before a clinically measurable deterioration of subjective hearing threshold. This so-called “hidden” hearing loss is characterized by speech comprehension difficulties. We examined young, middle-aged, and older individuals with and without hearing loss using pure-tone (PT) audiometry, short-pulsed distortion-product otoacoustic emissions (DPOAE), auditory brainstem responses (ABR), auditory steady state responses (ASSR), speech comprehension (OLSA), and syllable discrimination in quiet and noise. After normalizing OLSA thresholds for PT thresholds (“PNOT”), differences in speech comprehension still remained and showed no significant dependence on age, allowing us to categorize participants into groups with good, standard, and poor speech comprehension. Listeners with poor speech comprehension in quiet exhibited smaller firing rate adaptions at stimulus onset (as measured by the difference between DPOAE threshold and pure-tone threshold) and delayed supra-threshold ABR waves I-V, suggesting high spontaneous rate low threshold fiber cochlear synaptopathy. In contrast, when speech comprehension was tested in noise, listeners with poor speech comprehension had larger DPOAEs acceptance rate, putatively resulting from altered basilar membrane compression (recruitment). This was linked with higher uncomfortable loudness levels and larger ASSR amplitudes. Moreover, performance in phoneme discrimination was significantly different below (/o/-/u/) and above the phase-locking limit (/i/-/y/), depending on whether vowels were presented in quiet or ipsilateral noise. This suggests that neural firing rate adaptation at stimulus onset is critical for speech comprehension, independent of hearing threshold and age, whereas the recruitment phenomenon counterbalances the loss in speech-in-noise discrimination due to impaired threshold.Significance StatementAge-related hearing loss is the third largest modifiable risk factor for cognitive decline. It has been suggested that the link between hearing loss and cognitive decline is not fully explained by hearing threshold loss. We here suggest that language comprehension deficits may be used as an early indication of future hearing loss and therefore cognitive decline. We found that, independent of age and pure-tone thresholds, speech comprehension in quiet and ipsilateral noise depend on different onset firing-rate adaptations of inner hair cells (measured by DPOAE threshold), along with cochlear synaptopathy of high spontaneous rate auditory nerve fibers and neural spiking synchronicity. These measures may be used as possible future indicators of risk for cognitive decline.

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Section: Discussionsupporting

confidence: 84%

Neural adaptation at stimulus onset and speed of neural processing as critical contributors to speech comprehension independent of hearing threshold or age

Schirmer,

Wolpert,

Dapper

et al. 2023

Preprint

View full text Add to dashboard Cite

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“…To address temporal acuity, we used a gap-in-noise auditory steady-state response (gap-ASSR) paradigm. 76 The gap-ASSR elicits a steady-state response by presenting short gaps in continuous noise at 40 Hz. Using short gap widths and shallow-amplitude modulation depths (~75%), we compared the limits of temporal processing of cortical circuits across experimental groups.…”

Section: Resultsmentioning

confidence: 99%

“…The EEG recording set-up has been previously reported. 76 Briefly, the attached cable was connected via a commutator to a TDT (Tucker Davis Technologies, FL) RA4LI/RA4PA headstage/pre-amp, which was connected to a TDT RZ6 multi-I/O processor. OpenEx (TDT) was used to simultaneously record EEG signals and operate the LED light used to synchronize the video and waveform data.…”

Section: Methodsmentioning

confidence: 99%

Female-specific dysfunction of sensory neocortical circuits in a mouse model of autism mediated by mGluR5 and estrogen receptor α

Molinaro,

Bowles,

Croom

et al. 2024

Cell Reports

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“…To determine if there are sex-specific alterations in temporal processing, particularly with rapid gaps in sounds, we performed epidural EEG recordings on the auditory (AC) and frontal cortices (FC) in young (P21-23) NSE Pten KO mice. To address temporal acuity, we used a gap-in-noise auditory steady state response (gap-ASSR) paradigm 76 . The gap-ASSR elicits a stead state response by presenting short gaps in continuous noise at 40 Hz.…”

Section: Resultsmentioning

confidence: 99%

“…Mice were briefly anesthetized with isoflurane and attached to an EEG cable. The EEG recording set-up has been previously reported 76 . Briefly, the attached cable was connected via a commutator to a TDT (Tucker Davis Technologies, FL) RA4LI/RA4PA headstage/pre-amp, which was connected to a TDT RZ6 multi-I/O processor.…”

Section: Methods Detailsmentioning

confidence: 99%

Female specific dysfunction of sensory neocortical circuits in a mouse model of autism mediated by mGluR5 and Estrogen Receptor α

Molinaro,

Bowles,

Croom

et al. 2023

Preprint

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Autism manifests differently in males and females and the brain mechanisms that mediate these sex-dependent differences are unknown. Here, we demonstrate that deletion of the ASD-risk gene, Pten, in neocortical pyramidal neurons (NSE Pten KO) results in robust hyperexcitability of local neocortical circuits in female, but not male, mice, observed as prolonged, spontaneous persistent activity states (UP states). Circuit hyperexcitability in females is mediated by enhanced signaling of metabotropic glutamate receptor 5 (mGluR5) and estrogen receptor α (ERα) to ERK and de novo protein synthesis. In support of this idea, Pten deleted cortical neurons have a female-specific increase in mGluR5 levels and mGluR5-driven protein synthesis rates, mGluR5-ERα complexes are elevated in female cortex and genetic reduction of ERα in Pten KO cortical neurons rescues circuit excitability, protein synthesis rates and enhanced neuron size selectively in females. Abnormal timing and hyperexcitability of neocortical circuits in female NSE Pten KO mice are associated with deficits in temporal processing of sensory stimuli and social behaviors as well as mGluR5-dependent seizures. Female-specific cortical hyperexcitability and mGluR5-dependent seizures are also observed in a human disease relevant mouse model, germline Pten+/- mice. Our results reveal molecular mechanisms by which sex and a high impact ASD-risk gene interact to affect brain function and behavior.

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Age-related changes in event related potentials, steady state responses and temporal processing in the auditory cortex of mice with severe or mild hearing loss

Cited by 14 publications

References 81 publications

Neural adaptation at stimulus onset and speed of neural processing as critical contributors to speech comprehension independent of hearing threshold or age

Neural adaptation at stimulus onset and speed of neural processing as critical contributors to speech comprehension independent of hearing threshold or age

Female-specific dysfunction of sensory neocortical circuits in a mouse model of autism mediated by mGluR5 and estrogen receptor α

Female specific dysfunction of sensory neocortical circuits in a mouse model of autism mediated by mGluR5 and Estrogen Receptor α

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