scholarly journals Age-related decline in cochlear ribbon synapses and its relation to different metrics of auditory-nerve activity

2021 ◽  
Author(s):  
Friederike Steenken ◽  
Amarins N. Heeringa ◽  
Rainer Beutelmann ◽  
Lichun Zhang ◽  
Sonny Bovee ◽  
...  
Keyword(s):  
Auditory Nerve ◽  
Nerve Activity ◽  
Ribbon Synapses ◽  
Age Related

scholarly journals Synaptic Transmission at the Cochlear Nucleus Endbulb Synapse During Age-Related Hearing Loss in Mice

2005 ◽  
Vol 94 (3) ◽  
pp. 1814-1824 ◽  
Author(s):  
Yong Wang ◽  
Paul B. Manis
Keyword(s):  
Hearing Loss ◽  
Synaptic Transmission ◽  
Cochlear Nucleus ◽  
Auditory Nerve ◽  
High Frequency ◽  
Nerve Activity ◽  
Synaptic Release ◽  
Endbulb Of Held ◽  
Age Related ◽  
Age Related Hearing Loss

Age-related hearing loss (AHL) typically starts from high-frequency regions of the cochlea and over time invades lower-frequency regions. During this progressive hearing loss, sound-evoked activity in spiral ganglion cells is reduced. DBA mice have an early onset of AHL. In this study, we examined synaptic transmission at the endbulb of Held synapse between auditory nerve fibers and bushy cells in the anterior ventral cochlear nucleus (AVCN). Synaptic transmission in hearing-impaired high-frequency areas of the AVCN was altered in old DBA mice. The spontaneous miniature excitatory postsynaptic current (mEPSC) frequency was substantially reduced (about 60%), and mEPSCs were significantly slower (about 115%) and smaller (about 70%) in high-frequency regions of old (average age 45 days) DBA mice compared with tonotopically matched regions of young (average age 22 days) DBA mice. Moreover, synaptic release probability was about 30% higher in high-frequency regions of young DBA than that in old DBA mice. Auditory nerve–evoked EPSCs showed less rectification in old DBA mice, suggesting recruitment of GluR2 subunits into the AMPA receptor complex. No similar age-related changes in synaptic release or EPSCs were found in age-matched, normal hearing young and old CBA mice. Taken together, our results suggest that auditory nerve activity plays a critical role in maintaining normal synaptic function at the endbulb of Held synapse after the onset of hearing. Auditory nerve activity regulates both presynaptic (release probability) and postsynaptic (receptor composition and kinetics) function at the endbulb synapse after the onset of hearing.

Auditory-Nerve Responses in Mice with Noise-Induced Cochlear Synaptopathy

2021 ◽  
Author(s):  
Kirupa Suthakar ◽  
M. Charles Liberman
Keyword(s):  
Auditory Nerve ◽  
Guinea Pigs ◽  
Frequency Tuning ◽  
Tone Burst ◽  
Nerve Fibers ◽  
Ribbon Synapses ◽  
Age Related ◽  
Synaptic Markers ◽  
Basal Half ◽  
Masking Noise

Cochlear synaptopathy is the noise-induced or age-related loss of ribbon synapses between inner hair cells (IHCs) and auditory nerve fibers (ANFs), first reported in CBA/CaJ mice. Recordings from single ANFs in anaesthesized, noise-exposed guinea pigs suggested that neurons with low spontaneous rates (SRs) and high thresholds are more vulnerable than low-threshold, high-SR fibers. However, there is extensive post-exposure regeneration of ANFs in guinea pigs, but not in mice. Here, we exposed CBA/CaJ mice to octave-band noise and recorded sound-evoked and spontaneous activity from single ANFs at least 2 weeks later. Confocal analysis of cochleae immunostained for pre- and post-synaptic markers confirmed the expected loss of 40 - 50% of ANF synapses in the basal half of the cochlea, however, our data were not consistent with a selective loss of low-SR fibers. Rather they suggested a loss of both SR groups in synaptopathic regions. Single-fiber thresholds and frequency tuning recovered to pre-exposure levels however, response to tone bursts showed increased peak and steady-state firing rates as well as decreased jitter in first-spike latencies. This apparent gain-of-function increased the robustness of tone-burst responses in the presence of continuous masking noise. This study suggests that the nature of noise-induced synaptic damage varies between different species and that, in mouse, the noise-induced hyperexcitability seen in central auditory circuits is also observed at the level of the auditory nerve.

Age-Related and Noise-Induced Hearing Loss

2018 ◽  
pp. 162-188
Author(s):  
Ruili Xie ◽  
Tessa-Jonne F. Ropp ◽  
Michael R. Kasten ◽  
Paul B. Manis
Keyword(s):  
Hearing Loss ◽  
Auditory Nerve ◽  
Transmitter Release ◽  
Time Course ◽  
Functional Change ◽  
Noise Induced Hearing Loss ◽  
Nerve Activity ◽  
Auditory Periphery ◽  
Age Related ◽  
Age Related Hearing Loss

Hearing loss generally occurs in the auditory periphery but leads to changes in the central auditory system. Noise-induced hearing loss (NIHL) and age-related hearing loss (ARHL) affect neurons in the ventral cochlear nucleus (VCN) at both the cellular and systems levels. In response to a decrease in auditory nerve activity associated with hearing loss, the large synaptic endings of the auditory nerve, the endbulbs of Held, undergo simplification of their structure and the volume of the postsynaptic bushy neurons decreases. A major functional change shared by NIHL and ARHL is the development of asynchronous transmitter release at endbulb synapses during periods of high afferent firing. Compensatory adjustements in transmitter release, including changes in release probability and quantal content, have also been reported. The excitability of the bushy cells undergoes subtle changes in the long-term, although short-term, reversible changes in excitability may also occur. These changes are not consistently observed across all models of hearing loss, suggesting that the time course of hearing loss, and potential developmental effects, may influence endbulb transmission in multiple ways. NIHL can alter the representation of the loudness of tonal stimuli by VCN neurons and is accompanied by changes in spontaneous activity in VCN neurons. However, little is known about the representation of more complex stimuli. The relationship between mechanistic changes in VCN neurons with noise-induced or age-related hearing loss, the accompanying change in sensory coding, and the reversibility of changes with the reintroduction of auditory nerve activity are areas that deserve further thoughtful exploration.

scholarly journals Noise-induced and age-related hearing loss:  new perspectives and potential therapies

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 927 ◽  
Author(s):  
M Charles Liberman
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Sensorineural Hearing Loss ◽  
Hair Cells ◽  
Auditory Nerve ◽  
Cell Loss ◽  
Sensorineural Hearing ◽  
Hair Cell Loss ◽  
Age Related ◽  
Age Related Hearing Loss

The classic view of sensorineural hearing loss has been that the primary damage targets are hair cells and that auditory nerve loss is typically secondary to hair cell degeneration. Recent work has challenged that view. In noise-induced hearing loss, exposures causing only reversible threshold shifts (and no hair cell loss) nevertheless cause permanent loss of >50% of the synaptic connections between hair cells and the auditory nerve. Similarly, in age-related hearing loss, degeneration of cochlear synapses precedes both hair cell loss and threshold elevation. This primary neural degeneration has remained a “hidden hearing loss” for two reasons: 1) the neuronal cell bodies survive for years despite loss of synaptic connection with hair cells, and 2) the degeneration is selective for auditory nerve fibers with high thresholds. Although not required for threshold detection when quiet, these high-threshold fibers are critical for hearing in noisy environments. Research suggests that primary neural degeneration is an important contributor to the perceptual handicap in sensorineural hearing loss, and it may be key to the generation of tinnitus and other associated perceptual anomalies. In cases where the hair cells survive, neurotrophin therapies can elicit neurite outgrowth from surviving auditory neurons and re-establishment of their peripheral synapses; thus, treatments may be on the horizon.

Neural Presbyacusis in Humans Inferred from Age-Related Differences in Auditory Nerve Function and Structure

2021 ◽  
pp. JN-RM-1747-21
Author(s):  
Kelly C. Harris ◽  
Jayne B. Ahlstrom ◽  
James W. Dias ◽  
Lilyana B. Kerouac ◽  
Carolyn M. McClaskey ◽  
...  
Keyword(s):  
Auditory Nerve ◽  
Nerve Function ◽  
Age Related

Age-related insult of cochlear ribbon synapses: An early-onset contributor to D-galactose-induced aging in mice

2020 ◽  
Vol 133 ◽  
pp. 104649 ◽  
Author(s):  
Zheng-De Du ◽  
Shu-Guang Han ◽  
Teng-Fei Qu ◽  
Bin Guo ◽  
Shu-Kui Yu ◽  
...  
Keyword(s):  
Early Onset ◽  
Ribbon Synapses ◽  
Age Related

scholarly journals Influence of Sex and Age on Muscle Sympathetic Nerve Activity of Healthy Normotensive Adults

Hypertension ◽  
2020 ◽  
Vol 76 (3) ◽  
pp. 997-1005 ◽  
Author(s):  
Daniel A. Keir ◽  
Mark B. Badrov ◽  
George Tomlinson ◽  
Catherine F. Notarius ◽  
Derek S. Kimmerly ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Mass Index ◽  
Body Mass ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Systematic Change ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Age Related

As with blood pressure, age-related changes in muscle sympathetic nerve activity (MSNA) may differ nonlinearly between sexes. Data acquired from 398 male (age: 39±17; range: 18–78 years [mean±SD]) and 260 female (age: 37±18; range: 18–81 years) normotensive healthy nonmedicated volunteers were analyzed using linear regression models with resting MSNA burst frequency as the outcome and the predictors sex, age, MSNA, blood pressure, and body mass index modelled with natural cubic splines. Age and body mass index contributed 41% and 11%, respectively, of MSNA variance in females and 23% and 1% in males. Overall, changes in MSNA with age were sigmoidal. At age 20, mean MSNA of males and females were similar, then diverged significantly, reaching in women a nadir at age 30. After 30, MSNA increased nonlinearly in both sexes. Both MSNA discharge and blood pressure were lower in females until age 50 (17±9 versus 25±10 bursts·min −1 ; P <1×10 −19 ; 106±11/66±8 versus 116±7/68±9 mm Hg; P <0.01) but converged thereafter (38±11 versus 35±12 bursts·min −1 ; P =0.17; 119±15/71±13 versus 120±13/72±9 mm Hg; P >0.56). Compared with age 30, MSNA burst frequency at age 70 was 57% higher in males but 3-fold greater in females; corresponding increases in systolic blood pressure were 1 (95% CI, −4 to 5) and 12 (95% CI, 6–16) mm Hg. Except for concordance in females beyond age 40, there was no systematic change with age in any resting MSNA-blood pressure relationship. In normotensive adults, MSNA increases after age 30, with ascendance steeper in women.

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