Differential Impact of Temporary and Permanent Noise-Induced Hearing Loss on Neuronal Cell Density in the Mouse Central Auditory Pathway

2010 ◽  
Vol 27 (8) ◽  
pp. 1499-1507 ◽  
Author(s):  
Moritz Gröschel ◽  
Romy Götze ◽  
Arne Ernst ◽  
Dietmar Basta
Keyword(s):  
Hearing Loss ◽  
Cell Density ◽  
Neuronal Cell ◽  
Auditory Pathway ◽  
Noise Induced Hearing Loss ◽  
Differential Impact ◽  
Central Auditory Pathway

scholarly journals Changes in microRNA Expression in the Cochlear Nucleus and Inferior Colliculus after Acute Noise-Induced Hearing Loss

2020 ◽  
Vol 21 (22) ◽  
pp. 8792
Author(s):  
Sohyeon Park ◽  
Seung Hee Han ◽  
Byeong-Gon Kim ◽  
Myung-Whan Suh ◽  
Jun Ho Lee ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Inferior Colliculus ◽  
Neural Plasticity ◽  
Cochlear Nucleus ◽  
Organ Of Corti ◽  
Auditory Pathway ◽  
Noise Induced Hearing Loss ◽  
Candidate Mirnas ◽  
Central Auditory Pathway

Noise-induced hearing loss (NIHL) can lead to secondary changes that induce neural plasticity in the central auditory pathway. These changes include decreases in the number of synapses, the degeneration of auditory nerve fibers, and reorganization of the cochlear nucleus (CN) and inferior colliculus (IC) in the brain. This study investigated the role of microRNAs (miRNAs) in the neural plasticity of the central auditory pathway after acute NIHL. Male Sprague–Dawley rats were exposed to white band noise at 115 dB for 2 h, and the auditory brainstem response (ABR) and morphology of the organ of Corti were evaluated on days 1 and 3. Following noise exposure, the ABR threshold shift was significantly smaller in the day 3 group, while wave II amplitudes were significantly larger in the day 3 group compared to the day 1 group. The organ of Corti on the basal turn showed evidence of damage and the number of surviving outer hair cells was significantly lower in the basal and middle turn areas of the hearing loss groups relative to controls. Five and three candidate miRNAs for each CN and IC were selected based on microarray analysis and quantitative reverse transcription PCR (RT-qPCR). The data confirmed that even short-term acoustic stimulation can lead to changes in neuroplasticity. Further studies are needed to validate the role of these candidate miRNAs. Such miRNAs may be used in the early diagnosis and treatment of neural plasticity of the central auditory pathway after acute NIHL.

Molecular and Structural Changes in the Cochlear Nucleus in Response to Hearing Loss

2018 ◽  
pp. 142-162
Author(s):  
Maria E. Rubio
Keyword(s):  
Hearing Loss ◽  
Cochlear Nucleus ◽  
Structural Changes ◽  
Auditory Pathway ◽  
The United States ◽  
Cellular Mechanisms ◽  
Auditory Experience ◽  
Central Auditory Pathway ◽  
The Brain

Hearing loss is the third most common health problem in the United States. It can affect the quality of life and relationships. About 48 million Americans have lost some hearing. Age, illness, and genetics contribute to the generation of hearing loss. During development, auditory synaptic circuitries are highly plastic and able to adapt to fluctuations in auditory experience. Whether this is so for mature auditory nerve synapses and circuitries within nuclei along the central auditory pathway is less understood. Daily fluctuations in auditory experience can lead to hearing deficits, including hearing loss and/or deafness, Therefore, understanding the cellular mechanisms that occur in mature central auditory synaptic circuitries that lead and/or contribute to hearing loss is important. This chapter focuses on published studies using animal models describing structural and molecular changes that occur in the cochlear nucleus in response to hearing loss, the first gateway of sound processing in the brain.

Review: Neural Mechanisms of Tinnitus and Hyperacusis in Acute Drug-Induced Ototoxicity

2021 ◽  
pp. 1-15
Author(s):  
Richard Salvi ◽  
Kelly Radziwon ◽  
Senthilvelan Manohar ◽  
Ben Auerbach ◽  
Dalian Ding ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Otoacoustic Emissions ◽  
Motor Planning ◽  
Auditory Pathway ◽  
Neural Mechanisms ◽  
High Dose ◽  
Neural Responses ◽  
Neural Signals ◽  
Drug Induced ◽  
Central Auditory Pathway

Purpose Tinnitus and hyperacusis are debilitating conditions often associated with age-, noise-, and drug-induced hearing loss. Because of their subjective nature, the neural mechanisms that give rise to tinnitus and hyperacusis are poorly understood. Over the past few decades, considerable progress has been made in deciphering the biological bases for these disorders using animal models. Method Important advances in understanding the biological bases of tinnitus and hyperacusis have come from studies in which tinnitus and hyperacusis are consistently induced with a high dose of salicylate, the active ingredient in aspirin. Results Salicylate induced a transient hearing loss characterized by a reduction in otoacoustic emissions, a moderate cochlear threshold shift, and a large reduction in the neural output of the cochlea. As the weak cochlear neural signals were relayed up the auditory pathway, they were progressively amplified so that the suprathreshold neural responses in the auditory cortex were much larger than normal. Excessive central gain (neural amplification), presumably resulting from diminished inhibition, is believed to contribute to hyperacusis and tinnitus. Salicylate also increased corticosterone stress hormone levels. Functional imaging studies indicated that salicylate increased spontaneous activity and enhanced functional connectivity between structures in the central auditory pathway and regions of the brain associated with arousal (reticular formation), emotion (amygdala), memory/spatial navigation (hippocampus), motor planning (cerebellum), and motor control (caudate/putamen). Conclusion These results suggest that tinnitus and hyperacusis arise from aberrant neural signaling in a complex neural network that includes both auditory and nonauditory structures.

scholarly journals Stroke-Associated Cortical Deafness: A Systematic Review of Clinical and Radiological Characteristics

2021 ◽  
Vol 11 (11) ◽  
pp. 1383
Author(s):  
Gracinda Silva ◽  
Rita Gonçalves ◽  
Isabel Taveira ◽  
Maria Mouzinho ◽  
Rui Osório ◽  
...  
Keyword(s):  
Systematic Review ◽  
Hearing Loss ◽  
Web Of Science ◽  
Oral Communication ◽  
Auditory Pathway ◽  
Severe Form ◽  
Mesh Terms ◽  
Bilateral Lesions ◽  
Central Auditory Pathway ◽  
Pure Word Deafness

Background: Stroke is the leading cause of cortical deafness (CD), the most severe form of central hearing impairment. CD remains poorly characterized and perhaps underdiagnosed. We perform a systematic review to describe the clinical and radiological features of stroke-associated CD. Methods: PubMed and the Web of Science databases were used to identify relevant publications up to 30 June 2021 using the MeSH terms: “deafness” and “stroke”, or “hearing loss” and “stroke” or “auditory agnosia” and “stroke”. Results: We found 46 cases, caused by bilateral lesions within the central auditory pathway, mostly located within or surrounding the superior temporal lobe gyri and/or the Heschl’s gyri (30/81%). In five (13.51%) patients, CD was caused by the subcortical hemispheric and in two (0.05%) in brainstem lesions. Sensorineural hearing loss was universal. Occasionally, a misdiagnosis by peripheral or psychiatric disorders occurred. A few (20%) had clinical improvement, with a regained oral conversation or evolution to pure word deafness (36.6%). A persistent inability of oral communication occurred in 43.3%. A full recovery of conversation was restricted to patients with subcortical lesions. Conclusions: Stroke-associated CD is rare, severe and results from combinations of cortical and subcortical lesions within the central auditory pathway. The recovery of functional hearing occurs, essentially, when caused by subcortical lesions.

Hearing Loss of a Central Type Secondary to Anoxic Anoxia

1976 ◽  
Vol 85 (6) ◽  
pp. 826-832 ◽  
Author(s):  
Kazumi Makishima ◽  
Roger B. Katz ◽  
James B. Snow
Keyword(s):  
Hearing Loss ◽  
Auditory Cortex ◽  
Inferior Colliculus ◽  
Guinea Pigs ◽  
Auditory Pathway ◽  
Threshold Sensitivity ◽  
Central Type ◽  
Acoustic Stimuli ◽  
Central Auditory Pathway ◽  
Relative Vulnerability

The effect of anoxic anoxia on the threshold sensitivity and amplitude of the responses from the auditory cortex, inferior colliculus and cochlea to acoustic stimuli in guinea pigs was studied. Decay of the amplitude of the responses from the auditory cortex and the inferior colliculus occurs faster and is more severe than that of the cochlea. Recovery of the amplitude of the responses is slower at the auditory cortex and the inferior colliculus than at the cochlea. Loss of auditory threshold sensitivity in anoxic anoxia is most prominent at the auditory cortex. The loss of sensitivity at the inferior colliculus is the next most severe. The loss of sensitivity at the cochlea is negligible. The relative vulnerability of the central auditory pathway to anoxic anoxia as compared to the end organ is demonstrated.

Differential effects of pannexins on noise-induced hearing loss

2016 ◽  
Vol 473 (24) ◽  
pp. 4665-4680 ◽  
Author(s):  
Julia M. Abitbol ◽  
John J. Kelly ◽  
Kevin Barr ◽  
Ashley L. Schormans ◽  
Dale W. Laird ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Noise Exposure ◽  
Morphological Changes ◽  
Cell Types ◽  
Auditory Pathway ◽  
Auditory Brainstem ◽  
Vital Role ◽  
Noise Induced Hearing Loss ◽  
Loud Noise ◽  
Brainstem Response

Hearing loss, including noise-induced hearing loss, is highly prevalent and severely hinders an individual's quality of life, yet many of the mechanisms that cause hearing loss are unknown. The pannexin (Panx) channel proteins, Panx1 and Panx3, are regionally expressed in many cell types along the auditory pathway, and mice lacking Panx1 in specific cells of the inner ear exhibit hearing loss, suggesting a vital role for Panxs in hearing. We proposed that Panx1 and/or Panx3 null mice would exhibit severe hearing loss and increased susceptibility to noise-induced hearing loss. Using the auditory brainstem response, we surprisingly found that Panx1−/− and Panx3−/− mice did not harbor hearing or cochlear nerve deficits. Furthermore, while Panx1−/− mice displayed no protection against loud noise-induced hearing loss, Panx3−/− mice exhibited enhanced 16- and 24-kHz hearing recovery 7 days after a loud noise exposure (NE; 12 kHz tone, 115 dB sound pressure level, 1 h). Interestingly, Cx26, Cx30, Cx43, and Panx2 were up-regulated in Panx3−/− mice compared with wild-type and/or Panx1−/− mice, and assessment of the auditory tract revealed morphological changes in the middle ear bones of Panx3−/− mice. It is unclear if these changes alone are sufficient to provide protection against loud noise-induced hearing loss. Contrary to what we expected, these data suggest that Panx1 and Panx3 are not essential for baseline hearing in mice tested, but the therapeutic targeting of Panx3 may prove protective against mid-high-frequency hearing loss caused by loud NE.

Comparing the electrophysiological effects of traumatic noise exposure between rodents

2022 ◽  
Author(s):  
Lenneke Kiefer ◽  
Lisa Koch ◽  
Melisa Merdan-Desik ◽  
Bernhard H. Gaese ◽  
Manuela Nowotny
Keyword(s):  
Hearing Loss ◽  
Noise Exposure ◽  
Temporal Dynamics ◽  
Auditory Pathway ◽  
Auditory Brainstem ◽  
Individual Variability ◽  
Rodent Species ◽  
Waveform Analysis ◽  
Auditory Brainstem Responses ◽  
Noise Induced Hearing Loss

Noise-induced hearing deficits are important health problems in the industrialized world. As the underlying physiological dysfunctions are not well understood, research in suitable animal models is urgently needed. Three rodent species (Mongolian gerbil, rat and mouse) were studied to compare the temporal dynamics of noise-induced hearing loss after identical procedures of noise exposure. Auditory brainstem responses (ABRs) were measured before, during and up to eight weeks after noise exposure for threshold determination and ABR waveform analysis. Trauma induction with stepwise increasing sound pressure level was interrupted by five interspersed ABR measurements. Comparing short- and long-term dynamics underlying the following noise-induced hearing loss revealed diverging time courses between the three species. Hearing loss occurred early on during noise exposure in all three rodent species at or above trauma frequency. Initial noise level (105 dB SPL) was most effective in rats while the delayed level-increase to 115 dB SPL affected mice much stronger. Induced temporary threshold shifts in rats and mice were larger in animals with lower pre-trauma ABR thresholds. The increase in activity (gain) along the auditory pathway was derived by comparing the amplitudes of short- and long-latency ABR waveform components. Directly after trauma, significant effects were found for rats (decreasing gain) and mice (increasing gain) while gerbils revealed high individual variability in gain changes. Taken together, our comparative study revealed pronounced species-specific differences in the development of noise-induced hearing loss and the related processing along the auditory pathway.

Ototoxic Effect of Erythromycin on Cochlear Potentials in the Guinea Pig

1997 ◽  
Vol 106 (7) ◽  
pp. 599-603 ◽  
Author(s):  
Toshimitsu Kobayashi ◽  
Daniel C. Marcus ◽  
You Rong ◽  
Kenji Ohyama ◽  
Toshihiko Chiba ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Guinea Pig ◽  
Stria Vascularis ◽  
Complete Recovery ◽  
Auditory Pathway ◽  
Cochlear Potentials ◽  
Maximum Decrease ◽  
First Time ◽  
Central Auditory Pathway ◽  
Cochlear Dysfunction

The mechanism of hearing loss due to the administration of intravenous erythromycin was investigated in the albino guinea pig, and it was found for the first time that this drug causes cochlear dysfunction. The endocochlear potential (EP) and the cochlear microphonics (CM) recorded at the first cochlear turn transiently decreased when erythromycin was administered intravenously at dosages of 100 and 150 mg/kg. The averaged maximum decrease in EP was 16 mV (n = 5) and 33 mV (n = 5) for 100 and 150 mg/kg, respectively. The maximum decrease in the CM was about 25% when the EP reached its lowest value with the injection of 150 mg/kg. A complete recovery of the EP and CM ensued within 20 minutes after each erythromycin dose. The perilymphatic perfusion of 3 mmol/L of erythromycin decreased the EP and CM; however, in contrast to the intravenous administration, the decrease of the CM was nearly complete and both the EP and CM were irreversible. Hearing loss due to intravenously administered erythromycin could likely be attributable to the transient dysfunction of the stria vascularis, although concomitant dysfunction of the central auditory pathway cannot be excluded.

For Those About to Rock

2012 ◽  
Vol 13 (1) ◽  
pp. 29-35
Author(s):  
Jennifer Tufts
Keyword(s):  
Hearing Loss ◽  
Cultural Landscape ◽  
Minimal Risk ◽  
Noise Induced Hearing Loss ◽  
Essential Information ◽  
Informed Decisions ◽  
Hearing Health ◽  
Loud Music ◽  
Protective Strategies

Loud music and noisy hobbies are part of our cultural landscape. These activities can be enjoyed with minimal risk to hearing if a few commonsense guidelines are followed. Educating clients about risks and protective strategies will empower them to make informed decisions about their hearing health that best reflect their values and priorities. In this article, the author covers essential information to avoiding noise-induced hearing loss, writing in easily accessible language to better help clinicians convey this information to their clients.

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