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

The miR-34a/Bcl-2 Pathway Contributes to Auditory Cortex Neuron Apoptosis in Age-Related Hearing Loss

2017 ◽  
Vol 22 (2) ◽  
pp. 96-103 ◽  
Author(s):  
Qiuhong Huang ◽  
Yongkang Ou ◽  
Hao Xiong ◽  
Haidi Yang ◽  
Zhigang Zhang ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Auditory Cortex ◽  
Molecular Mechanisms ◽  
Primary Auditory Cortex ◽  
Auditory Brainstem ◽  
Hearing Ability ◽  
Age Related ◽  
Brainstem Response ◽  
The Central Nervous System ◽  
Age Related Hearing Loss

Hypothesis: The miR-34a/Bcl-2 signaling pathway may play a role in the mechanisms related to age-related hearing loss (AHL) in the auditory cortex. Background: The auditory cortex plays a key role in the recognition and processing of complex sound. It is difficult to explain why patients with AHL have poor speech recognition, so increasing numbers of studies have focused on its central change. Although micro (mi)RNAs in the central nervous system have recently been increasingly reported to be associated with age-related diseases, the molecular mechanisms of AHL in the auditory cortex are not fully understood. Methods: The auditory brainstem response was used to assess the hearing ability of C57BL/6 mice, and q-PCR, immunohistochemistry, and Western blotting were used to detect the expression levels of miR-34a and Bcl-2 in the mouse auditory cortex. TUNEL and DNA fragmentation were adopted to detect the apoptosis of neurons in the auditory cortex. To verify the relationship of miR-34a and Bcl-2, we transfected an miR-34a mimic or miR-34a inhibitor into primary auditory cortex neurons. Results: In this study, miR-34a/Bcl-2 signaling was examined in auditory cortex neurons during aging. miR-34a and apoptosis increased in the auditory cortex neurons of C57BL/6 mice with aging, whereas an age-related decrease in Bcl-2 was determined. In the primary neurons of the auditory cortex, miR-34a overexpression inhibited Bcl-2, leading to an increase in apoptosis. Moreover, miR-34a knockdown increased Bcl-2 expression and diminished apoptosis. Conclusion: Our results support a link between age-related apoptosis in auditory cortex neurons and miR-34a/Bcl-2 signaling, which may serve as a potential mechanism of the expression of AHL in the auditory cortex.

scholarly journals Human Auditory Brainstem Response to Temporal Gaps in Noise

2001 ◽  
Vol 44 (4) ◽  
pp. 737-750 ◽  
Author(s):  
Lynne A. Werner ◽  
Richard C. Folsom ◽  
Lisa R. Mancl ◽  
Connie L. Syapin
Keyword(s):  
Hearing Loss ◽  
Auditory Brainstem Response ◽  
Detection Threshold ◽  
Auditory Brainstem ◽  
Normal Hearing ◽  
Broadband Noise ◽  
Gap Detection ◽  
Detection Thresholds ◽  
Brainstem Response ◽  
High Pass

Gap detection is a commonly used measure of temporal resolution, although the mechanisms underlying gap detection are not well understood. To the extent that gap detection depends on processes within, or peripheral to, the auditory brainstem, one would predict that a measure of gap threshold based on the auditory brainstem response (ABR) would be similar to the psychophysical gap detection threshold. Three experiments were performed to examine the relationship between ABR gap threshold and gap detection. Thresholds for gaps in a broadband noise were measured in young adults with normal hearing, using both psychophysical techniques and electrophysiological techniques that use the ABR. The mean gap thresholds obtained with the two methods were very similar, although ABR gap thresholds tended to be lower than psychophysical gap thresholds. There was a modest correlation between psychophysical and ABR gap thresholds across participants. ABR and psychophysical thresholds for noise masked by temporally continuous, high-pass, or spectrally notched noise were measured in adults with normal hearing. Restricting the frequency range with masking led to poorer gap thresholds on both measures. High-pass maskers affected the ABR and psychophysical gap thresholds similarly. Notched-noise-masked ABR and psychophysical gap thresholds were very similar except that low-frequency, notched-noise-masked ABR gap threshold was much poorer at low levels. The ABR gap threshold was more sensitive to changes in signal-to-masker ratio than was the psychophysical gap detection threshold. ABR and psychophysical thresholds for gaps in broadband noise were measured in listeners with sensorineural hearing loss and in infants. On average, both ABR gap thresholds and psychophysical gap detection thresholds of listeners with hearing loss were worse than those of listeners with normal hearing, although individual differences were observed. Psychophysical gap detection thresholds of 3- and 6-month-old infants were an order of magnitude worse than those of adults with normal hearing, as previously reported; however, ABR gap thresholds of 3-month-old infants were no different from those of adults with normal hearing. These results suggest that ABR gap thresholds and psychophysical gap detection depend on at least some of the same mechanisms within the auditory system.

scholarly journals Chronic Oral Selegiline Treatment Mitigates Age-Related Hearing Loss in BALB/c Mice

2021 ◽  
Vol 22 (6) ◽  
pp. 2853
Author(s):  
Judit Szepesy ◽  
Viktória Humli ◽  
János Farkas ◽  
Ildikó Miklya ◽  
Júlia Tímár ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Hearing Aids ◽  
Dose Range ◽  
Auditory Brainstem ◽  
High Frequency Hearing Loss ◽  
Age Related ◽  
Hearing Function ◽  
Brainstem Response ◽  
Aging Societies ◽  
Age Related Hearing Loss

Age-related hearing loss (ARHL), a sensorineural hearing loss of multifactorial origin, increases its prevalence in aging societies. Besides hearing aids and cochlear implants, there is no FDA approved efficient pharmacotherapy to either cure or prevent ARHL. We hypothesized that selegiline, an antiparkinsonian drug, could be a promising candidate for the treatment due to its complex neuroprotective, antioxidant, antiapoptotic, and dopaminergic neurotransmission enhancing effects. We monitored by repeated Auditory Brainstem Response (ABR) measurements the effect of chronic per os selegiline administration on the hearing function in BALB/c and DBA/2J mice, which strains exhibit moderate and rapid progressive high frequency hearing loss, respectively. The treatments were started at 1 month of age and lasted until almost a year and 5 months of age, respectively. In BALB/c mice, 4 mg/kg selegiline significantly mitigated the progression of ARHL at higher frequencies. Used in a wide dose range (0.15–45 mg/kg), selegiline had no effect in DBA/2J mice. Our results suggest that selegiline can partially preserve the hearing in certain forms of ARHL by alleviating its development. It might also be otoprotective in other mammals or humans.

scholarly journals Hormones and Hearing: Central Auditory Processing in Women

2019 ◽  
Vol 30 (06) ◽  
pp. 493-501
Author(s):  
Skylar Trott ◽  
Trey Cline ◽  
Jeffrey Weihing ◽  
Deidra Beshear ◽  
Matthew Bush ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Auditory Processing ◽  
Auditory Brainstem ◽  
Human Model ◽  
Central Auditory Processing ◽  
Hormonal Changes ◽  
Hearing Sensitivity ◽  
Organ Systems ◽  
Significant Difference ◽  
Brainstem Response

AbstractEstrogen has been identified as playing a key role in many organ systems. Recently, estrogen has been found to be produced in the human brain and is believed contribute to central auditory processing. After menopause, a low estrogen state, many women report hearing loss but demonstrate no deficits in peripheral hearing sensitivity, which support the notion that estrogen plays an effect on central auditory processing. Although animal research on estrogen and hearing loss is extensive, there is little in the literature on the human model.The aim of this study was to evaluate relationships between hormonal changes and hearing as it relates to higher auditory function in pre- and postmenopausal (Post-M) females.A prospective, group comparison study.Twenty eight women between the ages of 18 and 70 at the University of Kentucky were recruited.Participants were separated into premenopausal and peri-/Post-M groups. Participants had normal peripheral hearing sensitivity and underwent a behavioral auditory processing battery and electrophysiological evaluation. An analysis of variance was performed to address the aims of the study.Results from the study demonstrated statistically significant difference between groups, where Post-M females had difficulties in spatial hearing abilities as reflected on the Listening in Spatialized Noise Test–Sentences test. In addition, measures on the auditory brainstem response and the middle latency response reflected statistically significant differences between groups with Post-M females having longer latencies.Results from the present study demonstrated significant differences between groups, particularly listening in noise. Females who present with auditory complaints in spite of normal hearing thresholds should have a more extensive audiological evaluation to further evaluate possible central deficits.

scholarly journals Deletion of Oncomodulin Gives Rise to Early Progressive Cochlear Dysfunction in C57 and CBA Mice

2021 ◽  
Vol 13 ◽  
Author(s):  
Leslie K. Climer ◽  
Aubrey J. Hornak ◽  
Kaitlin Murtha ◽  
Yang Yang ◽  
Andrew M. Cox ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Cell Function ◽  
Otoacoustic Emission ◽  
Cell Types ◽  
Auditory Brainstem ◽  
Outer Hair Cells ◽  
Distortion Product Otoacoustic Emission ◽  
Distortion Product ◽  
Age Related ◽  
Brainstem Response

Ca2+ signaling is a major contributor to sensory hair cell function in the cochlea. Oncomodulin (OCM) is a Ca2+ binding protein (CaBP) preferentially expressed in outer hair cells (OHCs) of the cochlea and few other specialized cell types. Here, we expand on our previous reports and show that OCM delays hearing loss in mice of two different genetic backgrounds: CBA/CaJ and C57Bl/6J. In both backgrounds, genetic disruption of Ocm leads to early progressive hearing loss as measured by auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE). In both strains, loss of Ocm reduced hearing across lifetime (hearing span) by more than 50% relative to wild type (WT). Even though the two WT strains have very different hearing spans, OCM plays a considerable and similar role within their genetic environment to regulate hearing function. The accelerated age-related hearing loss (ARHL) of the Ocm KO illustrates the importance of Ca2+ signaling in maintaining hearing health. Manipulation of OCM and Ca2+ signaling may reveal important clues to the systems of function/dysfunction that lead to ARHL.

Presbyacusis and the Auditory Brainstem Response

2002 ◽  
Vol 45 (6) ◽  
pp. 1249-1261 ◽  
Author(s):  
Flint A. Boettcher
Keyword(s):  
Hearing Loss ◽  
Auditory System ◽  
Auditory Brainstem Response ◽  
Animal Studies ◽  
Auditory Brainstem ◽  
Clinical Tool ◽  
Age Related ◽  
Brainstem Response ◽  
Auditory Functions ◽  
Age Related Changes

Age-related hearing loss (ARHL or presbyacusis) is an increasingly common form of sensorineural hearing loss (SNHL) as a result of changing demographics, and the auditory brainstem response (ABR) is a common experimental and clinical tool in audiology and neurology. Some of the changes that occur in the aging auditory system may significantly influence the interpretation of the ABR in comparison to the ABRs of younger adults. The approach of this review will be to integrate physiological and histopathological data from human and animal studies to provide a better understanding of the array of age-related changes in the ABR and to determine how age-related changes in the auditory system may influence how the ABR should be interpreted in presbyacusis. Data will be described in terms of thresholds, latencies, and amplitudes, as well as more complex auditory functions such as masking and temporal processing. Included in the review of data will be an attempt to differentiate between age-related effects that may strictly be due to threshold elevation from those that may be due to the aging process.

scholarly journals Oncomodulin Delays Age-Related Hearing Loss in C57 and CBA Mice

2021 ◽  
Author(s):  
Leslie K Climer ◽  
Aubrey J Hornak ◽  
Kaitlin Murtha ◽  
Yang Yang ◽  
Andrew M Cox ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Cell Function ◽  
Otoacoustic Emission ◽  
Auditory Brainstem ◽  
Outer Hair Cells ◽  
Distortion Product Otoacoustic Emission ◽  
Progressive Hearing Loss ◽  
Distortion Product ◽  
Age Related ◽  
Brainstem Response

Ca2+ signaling is a major contributor to sensory hair cell function in the cochlea. Oncomodulin (OCM) is a Ca2+ binding protein preferentially expressed in outer hair cells of the cochlea and few other specialized cell types. Here, we expand on our previous reports and show that OCM prevents early progressive hearing loss in mice of two different genetic backgrounds: CBA/CaJ and C57Bl/6J. In both backgrounds, genetic disruption of Ocm leads to early progressive hearing loss as measured by auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE). In both strains, loss of Ocm reduced hearing across lifetime (hearing span) by more than 50% relative to wild type (WT). Even though the two WT strains have very different hearing spans, OCM plays a considerable and similar role within their genetic environment to regulate hearing function. The accelerated ARHL of the Ocm KO illustrates the importance of Ca2+ signaling in maintaining hearing health.

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 Age-Related Hearing Loss in Mn-SOD Heterozygous Knockout Mice

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Makoto Kinoshita ◽  
Takashi Sakamoto ◽  
Akinori Kashio ◽  
Takahiko Shimizu ◽  
Tatsuya Yamasoba
Keyword(s):  
Hearing Loss ◽  
Manganese Superoxide Dismutase ◽  
Stria Vascularis ◽  
Spiral Ganglion ◽  
Cell Loss ◽  
Auditory Brainstem ◽  
Spiral Ganglion Cell ◽  
Age Related ◽  
Brainstem Response ◽  
Age Related Hearing Loss

Age-related hearing loss (AHL) reduces the quality of life for many elderly individuals. Manganese superoxide dismutase (Mn-SOD), one of the antioxidant enzymes acting within the mitochondria, plays a crucial role in scavenging reactive oxygen species (ROS). To determine whether reduction in Mn-SOD accelerates AHL, we evaluated auditory function in Mn-SOD heterozygous knockout (HET) mice and their littermate wild-type (WT) C57BL/6 mice by means of auditory brainstem response (ABR). Mean ABR thresholds were significantly increased at 16 months when compared to those at 4 months in both WT and HET mice, but they did not significantly differ between them at either age. The extent of hair cell loss, spiral ganglion cell density, and thickness of the stria vascularis also did not differ between WT and HET mice at either age. At 16 months, immunoreactivity of 8-hydroxydeoxyguanosine was significantly greater in the SGC and SV in HET mice compared to WT mice, but that of 4-hydroxynonenal did not differ between them. These findings suggest that, although decrease of Mn-SOD by half may increase oxidative stress in the cochlea to some extent, it may not be sufficient to accelerate age-related cochlear damage under physiological aging process.

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