scholarly journals Age-Dependent Auditory Processing Deficits after Cochlear Synaptopathy Depend on Auditory Nerve Latency and the Ability of the Brain to Recruit LTP/BDNF

2020 ◽  
Vol 10 (10) ◽  
pp. 710
Author(s):  
Philine Marchetta ◽  
Daria Savitska ◽  
Angelika Kübler ◽  
Giulia Asola ◽  
Marie Manthey ◽  
...  
Keyword(s):  
Temporal Processing ◽  
Auditory Processing ◽  
Auditory Nerve ◽  
Temporal Discrimination ◽  
Long Term Potentiation ◽  
Nerve Fibers ◽  
Age Related ◽  
Age Dependent ◽  
Processing Deficits ◽  
Neural Gain

Age-related decoupling of auditory nerve fibers from hair cells (cochlear synaptopathy) has been linked to temporal processing deficits and impaired speech recognition performance. The link between both is elusive. We have previously demonstrated that cochlear synaptopathy, if centrally compensated through enhanced input/output function (neural gain), can prevent age-dependent temporal discrimination loss. It was also found that central neural gain after acoustic trauma was linked to hippocampal long-term potentiation (LTP) and upregulation of brain-derived neurotrophic factor (BDNF). Using middle-aged and old BDNF-live-exon-visualization (BLEV) reporter mice we analyzed the specific recruitment of LTP and the activity-dependent usage of Bdnf exon-IV and -VI promoters relative to cochlear synaptopathy and central (temporal) processing. For both groups, specimens with higher or lower ability to centrally compensate diminished auditory nerve activity were found. Strikingly, low compensating mouse groups differed from high compensators by prolonged auditory nerve latency. Moreover, low compensators exhibited attenuated responses to amplitude-modulated tones, and a reduction of hippocampal LTP and Bdnf transcript levels in comparison to high compensators. These results suggest that latency of auditory nerve processing, recruitment of hippocampal LTP, and Bdnf transcription, are key factors for age-dependent auditory processing deficits, rather than cochlear synaptopathy or aging per se.

scholarly journals Disturbed Balance of Inhibitory Signaling Links Hearing Loss and Cognition

2022 ◽  
Vol 15 ◽  
Author(s):  
Marlies Knipper ◽  
Wibke Singer ◽  
Kerstin Schwabe ◽  
Gisela E. Hagberg ◽  
Yiwen Li Hegner ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Inhibitory Activity ◽  
Auditory Processing ◽  
Gain Control ◽  
Auditory Pathway ◽  
Adjustment Processes ◽  
Age Dependent ◽  
Inhibitory Strength ◽  
Processing Deficits ◽  
Neural Gain

Neuronal hyperexcitability in the central auditory pathway linked to reduced inhibitory activity is associated with numerous forms of hearing loss, including noise damage, age-dependent hearing loss, and deafness, as well as tinnitus or auditory processing deficits in autism spectrum disorder (ASD). In most cases, the reduced central inhibitory activity and the accompanying hyperexcitability are interpreted as an active compensatory response to the absence of synaptic activity, linked to increased central neural gain control (increased output activity relative to reduced input). We here suggest that hyperexcitability also could be related to an immaturity or impairment of tonic inhibitory strength that typically develops in an activity-dependent process in the ascending auditory pathway with auditory experience. In these cases, high-SR auditory nerve fibers, which are critical for the shortest latencies and lowest sound thresholds, may have either not matured (possibly in congenital deafness or autism) or are dysfunctional (possibly after sudden, stressful auditory trauma or age-dependent hearing loss linked with cognitive decline). Fast auditory processing deficits can occur despite maintained basal hearing. In that case, tonic inhibitory strength is reduced in ascending auditory nuclei, and fast inhibitory parvalbumin positive interneuron (PV-IN) dendrites are diminished in auditory and frontal brain regions. This leads to deficits in central neural gain control linked to hippocampal LTP/LTD deficiencies, cognitive deficits, and unbalanced extra-hypothalamic stress control. Under these conditions, a diminished inhibitory strength may weaken local neuronal coupling to homeostatic vascular responses required for the metabolic support of auditory adjustment processes. We emphasize the need to distinguish these two states of excitatory/inhibitory imbalance in hearing disorders: (i) Under conditions of preserved fast auditory processing and sustained tonic inhibitory strength, an excitatory/inhibitory imbalance following auditory deprivation can maintain precise hearing through a memory linked, transient disinhibition that leads to enhanced spiking fidelity (central neural gain⇑) (ii) Under conditions of critically diminished fast auditory processing and reduced tonic inhibitory strength, hyperexcitability can be part of an increased synchronization over a broader frequency range, linked to reduced spiking reliability (central neural gain⇓). This latter stage mutually reinforces diminished metabolic support for auditory adjustment processes, increasing the risks for canonical dementia syndromes.

R446 – Rostral Cochlear Nucleus Changes After Cochlear Ablation

2008 ◽  
Vol 139 (2_suppl) ◽  
pp. P194-P194 ◽  
Author(s):  
Kyle Robinson ◽  
Donald A Godfrey ◽  
Matthew A. Godfrey
Keyword(s):  
Auditory Processing ◽  
Cochlear Nucleus ◽  
Auditory Nerve ◽  
High Performance ◽  
Nerve Fibers ◽  
Average Concentration ◽  
Gamma Aminobutyric Acid ◽  
Freeze Dried ◽  
Concentration Changes ◽  
Temporal Bones

Problem Identification of neurotransmitter concentration changes occurring in the rostral anterior ventral cochlear nucleus (AVCN) following transection of the auditory nerve within the cochlea. Methods Chinchillas with cochlear ablations, as well as sham-lesioned chinchillas, were euthanized at times ranging from 3 to 84 days post ablation. Both temporal bones and brains were saved. Temporal bones were fixed, embedded in paraffin and sectioned to document the completeness of the cochlear lesion. Brain portions containing the cochlear nuclei were frozen-sectioned, and sections were freeze dried. Freeze-dried sections were microdissected into samples of AVCN for high performance liquid chromatography (HPLC) assay of 12 amino acid concentrations. Results The average concentration of glutamate, the most likely neurotransmitter of auditory nerve fibers, declined in the lesioned-side rostral AVCN by about 25% at 15 days. This decrease was maintained through 31 days post ablation and became bilateral at 83 days. There was no decrease in the adjacent granular region. Larger lesioned-side decreases, approaching 50%, were found more caudally in the AVCN at 31 days post ablation. The average concentration of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) decreased bilaterally by 15–25% at 3 through 15 days post ablation. Conclusion The degeneration of the central portion of the auditory nerve following mechanical ablation of the cochlea is accompanied by decreases of glutamate concentration on the lesioned side but bilateral decreases of GABA in the rostral part of the AVCN. These decreases were smaller than those reported previously for the posteroventral cochlear nucleus (PVCN). However, changes more caudally in AVCN approach those found in PVCN. Significance Our results are consistent with other evidence that damage to the cochlea leads to neurotransmitter changes in the central auditory system. The smaller changes in AVCN than in PVCN may correlate with different types of auditory processing in these two regions. Support The American Tinnitus Association and the University of Toledo Foundation.

scholarly journals Spermidine protects from age-related synaptic alterations at hippocampal mossy fiber-CA3 synapses

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Marta Maglione ◽  
Gaga Kochlamazashvili ◽  
Tobias Eisenberg ◽  
Bence Rácz ◽  
Eva Michael ◽  
...  
Keyword(s):  
Molecular Basis ◽  
Memory Impairment ◽  
Mossy Fiber ◽  
Long Term Potentiation ◽  
Age Related ◽  
Term Potentiation ◽  
Hippocampal Synapses ◽  
Age Dependent ◽  
Age Related Changes

AbstractAging is associated with functional alterations of synapses thought to contribute to age-dependent memory impairment (AMI). While therapeutic avenues to protect from AMI are largely elusive, supplementation of spermidine, a polyamine normally declining with age, has been shown to restore defective proteostasis and to protect from AMI in Drosophila. Here we demonstrate that dietary spermidine protects from age-related synaptic alterations at hippocampal mossy fiber (MF)-CA3 synapses and prevents the aging-induced loss of neuronal mitochondria. Dietary spermidine rescued age-dependent decreases in synaptic vesicle density and largely restored defective presynaptic MF-CA3 long-term potentiation (LTP) at MF-CA3 synapses (MF-CA3) in aged animals. In contrast, spermidine failed to protect CA3-CA1 hippocampal synapses characterized by postsynaptic LTP from age-related changes in function and morphology. Our data demonstrate that dietary spermidine attenuates age-associated deterioration of MF-CA3 synaptic transmission and plasticity. These findings provide a physiological and molecular basis for the future therapeutic usage of spermidine.

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.

scholarly journals Biased Auditory Nerve Central Synaptopathy Exacerbates Age-related Hearing Loss

2020 ◽  
Author(s):  
Meijian Wang ◽  
Chuangeng Zhang ◽  
Shengyin Lin ◽  
Yong Wang ◽  
Benjamin J. Seicol ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Auditory Processing ◽  
Auditory Nerve ◽  
Spiral Ganglion ◽  
Central Auditory Processing ◽  
Endbulb Of Held ◽  
Age Related ◽  
Central Synapses ◽  
Ganglion Neurons ◽  
Age Related Hearing Loss

SUMMARYSound information is transmitted from the cochlea to the brain by different subtypes of spiral ganglion neurons (SGN), which show varying degrees of vulnerbility under pathological conditions. It remains unclear how information from these SGNs reassemble among target neurons in the cochlear nucleus (CN) at the auditory nerve (AN) central synapses, and how different synapses change during hearing loss. Combining immunohistochemistry with electrophysiology, we investigated the giant endbulb of Held synapses and their postsynaptic bushy neurons in mice under normal hearing and age-related hearing loss (ARHL). We found that calretinin-expressing and non-calretinin-expressing endbulbs converge at continuously different ratios onto bushy neurons with varying physiological properties. Endbulbs degenerate during ARHL, and the degeneration is more severe in non-calretinin-expressing synapses, which correlates with a gradual decrease in neuronal subpopulation predominantly innervated by these inputs. Our findings suggest that biased AN central synaptopathy and shifted CN neuronal composition underlie reduced auditory input and altered central auditory processing during ARHL.

scholarly journals Pharmacological modulation of Kv3.1 mitigates auditory midbrain temporal processing deficits following auditory nerve damage

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Anna R. Chambers ◽  
Nadia Pilati ◽  
Pooja Balaram ◽  
Charles H. Large ◽  
Leonard K. Kaczmarek ◽  
...  
Keyword(s):  
Temporal Processing ◽  
Auditory Nerve ◽  
Nerve Damage ◽  
Auditory Midbrain ◽  
Pharmacological Modulation ◽  
Processing Deficits

scholarly journals Representation of speech in noise in the aging midbrain and cortex: aging may dominate over hearing-loss

2017 ◽  
Author(s):  
Alessandro Presacco ◽  
Jonathan Z. Simon ◽  
Samira Anderson
Keyword(s):  
Older Adults ◽  
Hearing Loss ◽  
Sensorineural Hearing Loss ◽  
Temporal Processing ◽  
Normal Hearing ◽  
Sensorineural Hearing ◽  
Speech In Noise ◽  
Age Related ◽  
Cortical Responses ◽  
Processing Deficits

ABSTRACTObjectiveTo understand the effect of peripheral hearing loss on the representation of speech in noise in the aging midbrain and cortex.MethodsSubjects comprised 17 normal-hearing younger adults, 15 normal-hearing older adults and 14 hearing-impaired older adults. The midbrain response, measured with Frequency-Following Responses (FFRs), and the cortical response, measured with magnetoencephalography (MEG) responses, were recorded from subjects listening to speech in quiet and noise at varying signal to noise ratios (SNRs).ResultsBoth groups of older listeners showed both weaker midbrain response amplitudes and overrepresentation of cortical responses compared to younger listeners. However, significant differences between the older groups were found in both midbrain-cortex relationships and in cortical processing durations, suggesting that hearing loss may alter reciprocal connections between lower and higher levels of the auditory pathway.ConclusionsThe paucity of differences in midbrain or cortical responses between the two older groups suggest that age-related temporal processing deficits may contribute to older adults’ communication difficulties beyond what might be predicted from peripheral hearing loss alone.SignificanceClinical devices, such as hearing aids, should not ignore age-related temporal processing deficits in the design of algorithms to maximize user benefit.HIGHLIGHTSMild sensorineural hearing loss does not appear to significantly exacerbate already appreciable age-related deficits in midbrain speech-in-noise encoding.Mild sensorineural hearing loss also does not appear to significantly exacerbate already appreciable age-related deficits in most measures of cortical speech-in-noise encoding.Central processing deficits caused by peripheral hearing loss in older adults are seen only in more subtle measures, including altered relationships between midbrain and 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

Patterns of Auditory Processing and Articulation Deficits in Academically Deficient Juvenile Delinquents

1983 ◽  
Vol 48 (1) ◽  
pp. 36-40 ◽  
Author(s):  
Peter W. Zinkus ◽  
Marvin I. Gottlieb
Keyword(s):  
Auditory Processing ◽  
Juvenile Delinquents ◽  
Language Disorders ◽  
Treatment Programs ◽  
Early School ◽  
Articulation Disorders ◽  
Processing Deficits ◽  
Academically Deficient ◽  
School Period ◽  
Speech And Language Disorders

Auditory processing deficits and articulation disorders were studied in a group of male juvenile delinquents. Significant auditory processing deficits were frequently observed and were significantly related to underachievement in reading, spelling, and arithmetic. In addition, articulation disorders were present in over 60% of the delinquent subjects. The results are interpreted to indicate that the evaluation of speech capabilities and auditory processing skills should be an integral part of treatment programs for delinquent populations. The importance of early intervention through identification and treatment of speech and language disorders in the early school period is supported.

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