Comparison of temporal processing in the auditory brainstem neurons between acoustic and electrical hearing

2018 ◽  
Vol 143 (3) ◽  
pp. 1783-1784
Author(s):  
Michaela Müller ◽  
Barbara Beiderbeck ◽  
Benedikt Grothe ◽  
Michael Pecka
Keyword(s):  
Temporal Processing ◽  
Auditory Brainstem

scholarly journals The Role of Cognition in Common Measures of Peripheral Synaptopathy and Hidden Hearing Loss

2019 ◽  
Vol 28 (4) ◽  
pp. 843-856 ◽  
Author(s):  
Aryn M. Kamerer ◽  
Angela AuBuchon ◽  
Sara E. Fultz ◽  
Judy G. Kopun ◽  
Stephen T. Neely ◽  
...  
Keyword(s):  
Temporal Processing ◽  
Cognitive Abilities ◽  
Working Memory Capacity ◽  
Detection Threshold ◽  
Auditory Brainstem ◽  
Cognitive Capacity ◽  
Healthy Population ◽  
Hearing Disorder ◽  
Hearing Sensitivity ◽  
Brainstem Response

Purpose The aim of this study was to quantify the portion of variance in several measures suggested to be indicative of peripheral noise-induced cochlear synaptopathy and hidden hearing disorder that can be attributed to individual cognitive capacity. Method Regression and relative importance analysis was used to model several behavioral and physiological measures of hearing in 32 adults ranging in age from 20 to 74 years. Predictors for the model were hearing sensitivity and performance on a number of cognitive tasks. Results There was a significant influence of cognitive capacity on several measures of cochlear synaptopathy and hidden hearing disorder. These measures include frequency modulation detection threshold, time-compressed word recognition in quiet and reverberation, and the strength of the frequency-following response of the speech-evoked auditory brainstem response. Conclusions Measures of hearing that involve temporal processing are significantly influenced by cognitive abilities, specifically, short-term and working memory capacity, executive function, and attention. Research using measures of temporal processing to diagnose peripheral disorders, such as noise-induced synaptopathy, need to consider cognitive influence even in a young, healthy population.

scholarly journals Developmental deprivation-induced perceptual and cortical processing deficits in awake-behaving animals

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Justin D Yao ◽  
Dan H Sanes
Keyword(s):  
Hearing Loss ◽  
Auditory Cortex ◽  
Temporal Processing ◽  
Sensory Deprivation ◽  
Auditory Brainstem ◽  
Auditory Task ◽  
Behavioral Deficits ◽  
Nervous System Function ◽  
The Relationship ◽  
Conductive Hearing

Sensory deprivation during development induces lifelong changes to central nervous system function that are associated with perceptual impairments. However, the relationship between neural and behavioral deficits is uncertain due to a lack of simultaneous measurements during task performance. Therefore, we telemetrically recorded from auditory cortex neurons in gerbils reared with developmental conductive hearing loss as they performed an auditory task in which rapid fluctuations in amplitude are detected. These data were compared to a measure of auditory brainstem temporal processing from each animal. We found that developmental HL diminished behavioral performance, but did not alter brainstem temporal processing. However, the simultaneous assessment of neural and behavioral processing revealed that perceptual deficits were associated with a degraded cortical population code that could be explained by greater trial-to-trial response variability. Our findings suggest that the perceptual limitations that attend early hearing loss are best explained by an encoding deficit in auditory cortex.

scholarly journals Ultra-fine temporal resolution in auditory processing is preserved in aged mice without peripheral hearing loss

2018 ◽  
Author(s):  
Lasse Osterhagen ◽  
K. Jannis Hildebrandt
Keyword(s):  
Hearing Loss ◽  
Auditory Cortex ◽  
Temporal Processing ◽  
Auditory Processing ◽  
Auditory Brainstem ◽  
Neural Representation ◽  
Gap Detection ◽  
Detection Thresholds ◽  
Age Related ◽  
Brainstem Response

AbstractAge-related hearing loss (presbycusis) is caused by damage to the periphery as well as deterioration of central auditory processing. Gap detection is a paradigm to study age-related temporal processing deficits, which is assumed to be determined primarily by the latter. However, peripheral hearing loss is a strong confounding factor when using gap detection to measure temporal processing. In this study, we used mice from the CAST line, which is known to maintain excellent peripheral hearing, to rule out any contribution of peripheral hearing loss to gap detection performance. We employed an operant Go/No-go paradigm to obtain psychometric functions of gap in noise (GIN) detection at young and middle age. Besides, we measured auditory brainstem responses (ABR) and multiunit recordings in the auditory cortex (AC) in order to disentangle the processing stages of gap detection. We found detection thresholds around 0.6 ms in all measurement modalities. Detection thresholds did not increase with age. In the ABR, GIN stimuli are coded as onset responses to the noise that follows the gap, strikingly similar to the ABR of noise bursts in silence (NBIS). The simplicity of the neural representation of the gap together with the preservation of detection threshold in aged CAST mice suggests that GIN detection in the mouse is primarily determined by peripheral, not central processing.AbbreviaionsGINgap in noiseABRauditory brainstem responseACauditory cortexNBISnoise burst in silenceIINinhibitory interneuron

scholarly journals Nicotinic acetylcholine receptor subunit α7-knockout mice exhibit degraded auditory temporal processing

2019 ◽  
Vol 122 (2) ◽  
pp. 451-465 ◽  
Author(s):  
Richard A. Felix ◽  
Vicente A. Chavez ◽  
Dyana M. Novicio ◽  
Barbara J. Morley ◽  
Christine V. Portfors
Keyword(s):  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Temporal Processing ◽  
Knockout Mice ◽  
Auditory Processing ◽  
Auditory Brainstem ◽  
Spike Timing ◽  
Nicotinic Acetylcholine ◽  
Timing Delay ◽  
Knockout Animals

The CHRNA7 gene that encodes the α7-subunit of the nicotinic acetylcholine receptor (α7-nAChR) has been associated with some autism spectrum disorders and other neurodevelopmental conditions characterized, in part, by auditory and language impairment. These conditions may include auditory processing disorders that represent impaired timing of neural activity, often accompanied by problems understanding speech. Here, we measure timing properties of sound-evoked activity via the auditory brainstem response (ABR) of α7-nAChR knockout mice of both sexes and wild-type colony controls. We find a significant timing delay in evoked ABR signals that represents midbrain activity in knockouts. We also examine spike-timing properties of neurons in the inferior colliculus, a midbrain nucleus that exhibits high levels of α7-nAChR during development. We find delays of evoked responses along with degraded spiking precision in knockout animals. We find similar timing deficits in responses of neurons in the superior paraolivary nucleus and ventral nucleus of the lateral lemniscus, which are brainstem nuclei thought to shape temporal precision in the midbrain. In addition, we find that other measures of temporal acuity including forward masking and gap detection are impaired for knockout animals. We conclude that altered temporal processing at the level of the brainstem in α7-nAChR-deficient mice may contribute to degraded spike timing in the midbrain, which may underlie the observed timing delay in the ABR signals. Our findings are consistent with a role for the α7-nAChR in types of neurodevelopmental and auditory processing disorders and we identify potential neural targets for intervention. NEW & NOTEWORTHY Disrupted signaling via the α7-nicotinic acetylcholine receptor (α7-nAChR) is associated with neurodevelopmental disorders that include impaired auditory processing. The underlying causes of dysfunction are not known but a common feature is abnormal timing of neural activity. We examined temporal processing of α7-nAChR knockout mice and wild-type controls. We found degraded spike timing of neurons in knockout animals, which manifests at the level of the auditory brainstem and midbrain.

scholarly journals Temporal processing in the auditory brainstem response by full-term 6-week- and 9-month-old infants

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Xiaoqin Mai ◽  
Twila Tardif ◽  
Lin Xu ◽  
Mingyan Li ◽  
Paul R. Kileny ◽  
...  
Keyword(s):  
Temporal Processing ◽  
Auditory Brainstem Response ◽  
Auditory Brainstem ◽  
Full Term ◽  
Brainstem Response

scholarly journals Auditory Brainstem Response to Paired Click Stimulation as an Indicator of Peripheral Synaptic Health in Noise-Induced Cochlear Synaptopathy

2021 ◽  
Vol 14 ◽  
Author(s):  
Jae-Hun Lee ◽  
Min Young Lee ◽  
Ji Eun Choi ◽  
Jae Yun Jung
Keyword(s):  
Evoked Potentials ◽  
Hair Cells ◽  
Temporal Processing ◽  
Auditory Brainstem Response ◽  
Animal Studies ◽  
Auditory Evoked Potentials ◽  
Noise Exposure ◽  
Auditory Brainstem ◽  
Ribbon Synapses ◽  
Brainstem Response

IntroductionA defect in the cochlear afferent synapse between the inner hair cells and spiral ganglion neurons, after noise exposure, without changes in the hearing threshold has been reported. Animal studies on auditory evoked potentials demonstrated changes in the auditory brainstem response (ABR) measurements of peak I amplitude and the loss of synapses, which affect the temporal resolution of complex sounds. Human studies of auditory evoked potential have reported ambiguous results regarding the relationship between peak I amplitude and noise exposure. Paired click stimuli have been used to investigate the temporal processing abilities of humans and animals. In this study, we investigated the utility of measuring auditory evoked potentials in response to paired click stimuli to assess the temporal processing function of ribbon synapses in noise-induced cochlear synaptopathy.Materials and MethodsTwenty-two Sprague Dawley rats were used in this study, and synaptopathy was induced by narrow-band noise exposure (16 kHz with 1 kHz bandwidth, 105 dB sound pressure level for 2 h). ABRs to tone and paired click stimuli were measured before and 1, 3, 7, and 14 days after noise exposure. For histological analyses, hair cells and ribbon synapses were immunostained and the synapses quantified. The relationships among ABR peak I amplitude, number of synapses, and ABR to paired click stimuli were examined.ResultsOur results showed that ABR thresholds increase 1 day after noise exposure but fully recover to baseline levels after 14 days. Further, we demonstrated test frequency-dependent decreases in peak I amplitude and the number of synapses after noise exposure. These decreases were statistically significant at frequencies of 16 and 32 kHz. However, the ABR recovery threshold to paired click stimuli increased, which represent deterioration in the ability of temporal auditory processing. Our results indicate that the ABR recovery threshold is highly correlated with ABR peak I amplitude after noise exposure. We also established a direct correlation between the ABR recovery threshold and histological findings.ConclusionThe result from this study suggests that in animal studies, the ABR to paired click stimuli along with peak I amplitude has potential as an assessment tool for hidden hearing loss.

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