Auditory System: Deep Research from Cortex to Cochlea

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neurolinguistics".

Deadline for manuscript submissions: closed (25 July 2023) | Viewed by 3424

Special Issue Editors


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Guest Editor
1. Department of Otolaryngology, Clinical Hospital University of Chile, Santiago, Chile
2. Department of Neuroscience, Faculty of Medicine, University of Chile, Santiago, Chile
3. Advanced Center for Electrical and Electronic Engineering, AC3E, The Federico Santa María Technical University, Valparaíso, Chile
Interests: auditory efferent system; auditory perception, attention

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Guest Editor
Department of Otolaryngology-Head and Neck Surgery, The Center for Hearing and Balance, Johns Hopkins University School of Medicine, Baltimore, MD, USA
Interests: auditory evoked potentials; sensory and auditory neuroscience; hearing loss

Special Issue Information

Dear Colleagues,

A canonical view of the auditory system is centered on how diverse acoustic stimuli from the environment reach the cochlear receptor and through afferent pathways ascend in the central auditory pathways to reach the auditory cortex and non-acoustic neural networks.  However, neuroanatomical studies have evidenced numerous descending projections from the cortex to several subcortical auditory nuclei. These circuits can modulate the function of cochlear hair cells and auditory nerve fibers through a brainstem neural circuit composed by olivocochlear neurons. Therefore, a modern view of the functioning of the auditory system should include these efferent feedback loops that modulate afferent responses, to shape auditory perception. In this special issue, we invite researchers to submit original work and focused revisions in the auditory efferent system, including corticofugal and brainstem circuits to the cochlea.

Dr. Paul Hinckley Délano
Dr. Sergio Vicencio-Jimenez
Guest Editors

Manuscript Submission Information

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Keywords

  • auditory efferent
  • corticofugal
  • top-down
  • olivocochlear

Published Papers (2 papers)

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Research

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13 pages, 3803 KiB  
Article
Maintained Spatial Learning and Memory Functions in Middle-Aged α9 Nicotinic Receptor Subunit Knock-Out Mice
by Sergio Vicencio-Jimenez, Paul H. Delano, Natalia Madrid, Gonzalo Terreros, Juan C. Maass, Carolina Delgado and Pascal Jorratt
Brain Sci. 2023, 13(5), 794; https://doi.org/10.3390/brainsci13050794 - 12 May 2023
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Abstract
Age-related hearing loss is linked to cognitive impairment, but the mechanisms that relate to these conditions remain unclear. Evidence shows that the activation of medial olivocochlear (MOC) neurons delays cochlear aging and hearing loss. Consequently, the loss of MOC function may be related [...] Read more.
Age-related hearing loss is linked to cognitive impairment, but the mechanisms that relate to these conditions remain unclear. Evidence shows that the activation of medial olivocochlear (MOC) neurons delays cochlear aging and hearing loss. Consequently, the loss of MOC function may be related to cognitive impairment. The α9/α10 nicotinic receptor is the main target of cholinergic synapses between the MOC neurons and cochlear outer hair cells. Here, we explored spatial learning and memory performance in middle-aged wild-type (WT) and α9-nAChR subunit knock-out (KO) mice using the Barnes maze and measured auditory brainstem response (ABR) thresholds and the number of cochlear hair cells as a proxy of cochlear aging. Our results show non-significant spatial learning differences between WT and KO mice, but KO mice had a trend of increased latency to enter the escape box and freezing time. To test a possible reactivity to the escape box, we evaluated the novelty-induced behavior using an open field and found a tendency towards more freezing time in KO mice. There were no differences in memory, ABR threshold, or the number of cochlear hair cells. We suggest that the lack of α9-nAChR subunit alters novelty-induced behavior, but not spatial learning in middle-aged mice, by a non-cochlear mechanism. Full article
(This article belongs to the Special Issue Auditory System: Deep Research from Cortex to Cochlea)
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Review

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15 pages, 4587 KiB  
Review
The Development of Speaking and Singing in Infants May Play a Role in Genomics and Dementia in Humans
by Ebenezer N. Yamoah, Gabriela Pavlinkova and Bernd Fritzsch
Brain Sci. 2023, 13(8), 1190; https://doi.org/10.3390/brainsci13081190 - 11 Aug 2023
Cited by 1 | Viewed by 1501
Abstract
The development of the central auditory system, including the auditory cortex and other areas involved in processing sound, is shaped by genetic and environmental factors, enabling infants to learn how to speak. Before explaining hearing in humans, a short overview of auditory dysfunction [...] Read more.
The development of the central auditory system, including the auditory cortex and other areas involved in processing sound, is shaped by genetic and environmental factors, enabling infants to learn how to speak. Before explaining hearing in humans, a short overview of auditory dysfunction is provided. Environmental factors such as exposure to sound and language can impact the development and function of the auditory system sound processing, including discerning in speech perception, singing, and language processing. Infants can hear before birth, and sound exposure sculpts their developing auditory system structure and functions. Exposing infants to singing and speaking can support their auditory and language development. In aging humans, the hippocampus and auditory nuclear centers are affected by neurodegenerative diseases such as Alzheimer’s, resulting in memory and auditory processing difficulties. As the disease progresses, overt auditory nuclear center damage occurs, leading to problems in processing auditory information. In conclusion, combined memory and auditory processing difficulties significantly impact people’s ability to communicate and engage with their societal essence. Full article
(This article belongs to the Special Issue Auditory System: Deep Research from Cortex to Cochlea)
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