Special Issue "Central Auditory Plasticity"

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

Deadline for manuscript submissions: closed (25 March 2020).

Special Issue Editor

Dr. Maria E. Rubio
E-Mail Website
Guest Editor
Departments of Neurobiology and Otolaryngology, University of Pittsburgh, Pittsburgh, USA
Interests: hearing; hearing loss; synapses; tripartite synapse; glutamate receptors; synaptic plasticity; mechanisms of excitotoxicity; ultrastructure; immunolabeling

Special Issue Information

Dear Colleagues,

Currently, there is an increasing interest in understanding how, when, and for how long the adult central auditory system adapts to hearing loss. This interest has surged since adult auditory central pathways stopped being thought of as a hardwired system, primarily specified and determined genetically and influenced by sensory experience only during "critical" periods during development.

Central auditory plasticity can occur from very rapid adaptation to long-term changes and varies depending on the history of the sensory input (ascending pathways) or the influence of attention, learning, and decision making (descending pathways). Despite continuous efforts, it is still unknown whether central auditory plasticity to hearing loss represents homeostatic mechanisms or maladaptive changes that lead to tinnitus and hyperacusis.

We invite contributions of original research and reviews to this Special Issue of Brain Sciences entitled "Central Auditory Plasticity", the scope of which encompasses research relevant to the advancement of our understanding of the neurobiology underlying structural, molecular, electrophysiological, and behavioral adaptations to hearing loss.

Prof. Maria E. Rubio
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • hearing loss
  • conductive hearing loss
  • noise induced hearing loss
  • brainstem, midbrain, thalamus
  • cortex
  • synapses
  • synaptic circuits
  • structure
  • electrophysiology
  • neurotransmitters
  • neurotransmitter receptors
  • ion channels
  • neurons
  • glial cells

Published Papers (10 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Editorial

Jump to: Research, Review

Editorial
Central Auditory Plasticity from Molecules to Behavior
Brain Sci. 2021, 11(5), 573; https://doi.org/10.3390/brainsci11050573 - 29 Apr 2021
Viewed by 292
Abstract
Understanding how, when, and for how long the adult central auditory system adapts to hearing loss and aging is an important topic that is currently studied across the globe [...] Full article
(This article belongs to the Special Issue Central Auditory Plasticity)

Research

Jump to: Editorial, Review

Article
Evaluating the Impact of Age, Acoustic Exposure, and Electrical Stimulation on Binaural Sensitivity in Adult Bilateral Cochlear Implant Patients
Brain Sci. 2020, 10(6), 406; https://doi.org/10.3390/brainsci10060406 - 26 Jun 2020
Cited by 1 | Viewed by 956
Abstract
Deafness in both ears is highly disruptive to communication in everyday listening situations. Many individuals with profound deafness receive bilateral cochlear implants (CIs) to gain access to spatial cues used in localization and speech understanding in noise. However, the benefit of bilateral CIs, [...] Read more.
Deafness in both ears is highly disruptive to communication in everyday listening situations. Many individuals with profound deafness receive bilateral cochlear implants (CIs) to gain access to spatial cues used in localization and speech understanding in noise. However, the benefit of bilateral CIs, in particular sensitivity to interaural time and level differences (ITD and ILDs), varies among patients. We measured binaural sensitivity in 46 adult bilateral CI patients to explore the relationship between binaural sensitivity and three classes of patient-related factors: age, acoustic exposure, and electric hearing experience. Results show that ILD sensitivity increased with shorter years of acoustic exposure, younger age at testing, or an interaction between these factors, moderated by the duration of bilateral hearing impairment. ITD sensitivity was impacted by a moderating effect between years of bilateral hearing impairment and CI experience. When age at onset of deafness was treated as two categories (<18 vs. >18 years of age), there was no clear effect for ILD sensitivity, but some differences were observed for ITD sensitivity. Our findings imply that maximal binaural sensitivity is obtained by listeners with a shorter bilateral hearing impairment, a longer duration of CI experience, and potentially a younger age at testing. 198/200. Full article
(This article belongs to the Special Issue Central Auditory Plasticity)
Show Figures

Figure 1

Article
Transient Conductive Hearing Loss Regulates Cross-Modal VGLUT Expression in the Cochlear Nucleus of C57BL/6 Mice
Brain Sci. 2020, 10(5), 260; https://doi.org/10.3390/brainsci10050260 - 29 Apr 2020
Cited by 5 | Viewed by 1394
Abstract
Auditory nerve fibers synapse onto the cochlear nucleus (CN) and are labeled using the vesicular glutamate transporter-1 (VGLUT-1), whereas non-auditory inputs are labeled using the VGLUT-2. However, the underlying regulatory mechanism of VGLUT expression in the CN remains unknown. We examined whether a [...] Read more.
Auditory nerve fibers synapse onto the cochlear nucleus (CN) and are labeled using the vesicular glutamate transporter-1 (VGLUT-1), whereas non-auditory inputs are labeled using the VGLUT-2. However, the underlying regulatory mechanism of VGLUT expression in the CN remains unknown. We examined whether a sound level decrease, without primary neural damage, induces cellular and VGLUT expression change in the CN, and examined the potential for neural plasticity of the CN using unilateral conductive hearing loss models. We inserted earplugs in 8-week-old mice unilaterally for 4 weeks and subsequently removed them for another 4 weeks. Although the threshold of an auditory brainstem response significantly increased across all tested frequencies following earplug insertion, it completely recovered after earplug removal. Auditory deprivation had no significant impact on spiral ganglion and ventral CN (VCN) neurons’ survival. Conversely, although the cell size and VGLUT-1 expression in the VCN significantly decreased after earplug insertion, VGLUT-2 expression in the granule cell lamina significantly increased. These cell sizes decreased and the alterations in VGLUT-1 and -2 expression almost completely recovered at 1 month after earplug removal. Our results suggested that the cell size and VGLUT expression in the CN have a neuroplasticity capacity, which is regulated by increases and decreases in sound levels. Restoration of the sound levels might partly prevent cell size decrease and maintain VGLUT expression in the CN. Full article
(This article belongs to the Special Issue Central Auditory Plasticity)
Show Figures

Figure 1

Article
Bimodal Benefits for Lexical Tone Recognition: An Investigation on Mandarin-speaking Preschoolers with a Cochlear Implant and a Contralateral Hearing Aid
Brain Sci. 2020, 10(4), 238; https://doi.org/10.3390/brainsci10040238 - 17 Apr 2020
Cited by 3 | Viewed by 1163
Abstract
Pitch perception is known to be difficult for individuals with cochlear implant (CI), and adding a hearing aid (HA) in the non-implanted ear is potentially beneficial. The current study aimed to investigate the bimodal benefit for lexical tone recognition in Mandarin-speaking preschoolers using [...] Read more.
Pitch perception is known to be difficult for individuals with cochlear implant (CI), and adding a hearing aid (HA) in the non-implanted ear is potentially beneficial. The current study aimed to investigate the bimodal benefit for lexical tone recognition in Mandarin-speaking preschoolers using a CI and an HA in opposite ears. The child participants were required to complete tone identification in quiet and in noise with CI + HA in comparison with CI alone. While the bimodal listeners showed confusion between Tone 2 and Tone 3 in recognition, the additional acoustic information from the contralateral HA alleviated confusion between these two tones in quiet. Moreover, significant improvement was demonstrated in the CI + HA condition over the CI alone condition in noise. The bimodal benefit for individual subjects could be predicted by the low-frequency hearing threshold of the non-implanted ear and the duration of bimodal use. The findings support the clinical practice to fit a contralateral HA in the non-implanted ear for the potential benefit in Mandarin tone recognition in CI children. The limitations call for further studies on auditory plasticity on an individual basis to gain insights on the contributing factors to the bimodal benefit or its absence. Full article
(This article belongs to the Special Issue Central Auditory Plasticity)
Show Figures

Figure 1

Article
Expression and Localization of Kv1.1 and Kv3.1b Potassium Channels in the Cochlear Nucleus and Inferior Colliculus after Long-Term Auditory Deafferentation
Brain Sci. 2020, 10(1), 35; https://doi.org/10.3390/brainsci10010035 - 08 Jan 2020
Cited by 4 | Viewed by 1278
Abstract
Deafness affects the expression and distribution of voltage-dependent potassium channels (Kvs) of central auditory neurons in the short-term, i.e., hours to days, but the consequences in the expression of Kvs after long-term deafness remain unknown. We tested expression and distribution of Kv1.1 and [...] Read more.
Deafness affects the expression and distribution of voltage-dependent potassium channels (Kvs) of central auditory neurons in the short-term, i.e., hours to days, but the consequences in the expression of Kvs after long-term deafness remain unknown. We tested expression and distribution of Kv1.1 and Kv3.1b, key for auditory processing, in the rat cochlear nucleus (CN), and in the inferior colliculus (IC), at 1, 15 and 90 days after mechanical lesion of the cochlea, using a combination of qRT-PCR and Western blot in the whole CN, along with semi-quantitative immunocytochemistry in the AVCN, where the role of both Kvs in the control of excitability for accurate auditory timing signal processing is well established. Neither Kv1.1/Kv3.1b mRNA or protein expression changed significantly in the CN between 1 and 15 days after deafness. At 90 days post-lesion, however, mRNA and protein expression for both Kvs increased, suggesting that regulation of Kv1.1 and Kv3.1b expression is part of cellular mechanisms for long-term adaptation to auditory deprivation in the CN. Consistent with these findings, immunocytochemistry showed increased labeling intensity for both Kvs in the AVCN at day 90 after cochlear lesion. This increase argues that up-regulation of Kv1.1 and Kv3.1b in AVCN neurons may be required to adapt intrinsic excitability to altered input over the long term after auditory deprivation. Contrary to these findings in the CN, expression levels of Kv1.1 and Kv3.1b in the IC did not undergo major changes after cochlear lesion. In particular, there was no evidence of long-term up-regulation of either Kv1.1 or Kv3.1b, supporting that such post-lesion adaptive mechanism may not be needed in the IC. These results reveal that post-lesion adaptations do not necessarily involve stereotyped plastic mechanisms along the entire auditory pathway. Full article
(This article belongs to the Special Issue Central Auditory Plasticity)
Show Figures

Figure 1

Article
D-Stellate Neurons of the Ventral Cochlear Nucleus Decrease in Auditory Nerve-Evoked Activity during Age-Related Hearing Loss
Brain Sci. 2019, 9(11), 302; https://doi.org/10.3390/brainsci9110302 - 31 Oct 2019
Cited by 2 | Viewed by 964
Abstract
Age-related hearing loss (ARHL) is associated with weakened inhibition in the central auditory nervous system including the cochlear nucleus. One of the main inhibitory neurons of the cochlear nucleus is the D-stellate neuron, which provides extensive glycinergic inhibition within the local neural network. [...] Read more.
Age-related hearing loss (ARHL) is associated with weakened inhibition in the central auditory nervous system including the cochlear nucleus. One of the main inhibitory neurons of the cochlear nucleus is the D-stellate neuron, which provides extensive glycinergic inhibition within the local neural network. It remains unclear how physiological activities of D-stellate neurons change during ARHL and what are the underlying mechanisms. Using in vitro whole-cell patch clamp technique, we studied the intrinsic membrane properties of D-stellate neurons, the changes of their firing properties, and the underlying mechanisms in CBA/CaJ mice at the ages of 3–4 months (young), 17–19 months (middle age), and 27–33 months (aged). We found that the intrinsic membrane properties of D-stellate neurons were unchanged among these three age groups. However, these neurons showed decreased firing rate with age in response to sustained auditory nerve stimulation. Further investigation showed that auditory nerve-evoked excitatory postsynaptic currents (EPSCs) were significantly reduced in strength with age. These findings suggest that D-stellate neurons receive weakened synaptic inputs from the auditory nerve and decreased sound driven activity with age, which are expected to reduce the overall inhibition and enhance the central gain in the cochlear nucleus during ARHL. Full article
(This article belongs to the Special Issue Central Auditory Plasticity)
Show Figures

Figure 1

Review

Jump to: Editorial, Research

Review
Noise Induced Hearing Loss and Tinnitus—New Research Developments and Remaining Gaps in Disease Assessment, Treatment, and Prevention
Brain Sci. 2020, 10(10), 732; https://doi.org/10.3390/brainsci10100732 - 13 Oct 2020
Cited by 1 | Viewed by 1219
Abstract
Long-term noise exposure often results in noise induced hearing loss (NIHL). Tinnitus, the generation of phantom sounds, can also result from noise exposure, although understanding of its underlying mechanisms are limited. Recent studies, however, are shedding light on the neural processes involved in [...] Read more.
Long-term noise exposure often results in noise induced hearing loss (NIHL). Tinnitus, the generation of phantom sounds, can also result from noise exposure, although understanding of its underlying mechanisms are limited. Recent studies, however, are shedding light on the neural processes involved in NIHL and tinnitus, leading to potential new and innovative treatments. This review focuses on the assessment of NIHL, available treatments, and development of new pharmacologic and non-pharmacologic treatments based on recent studies of central auditory plasticity and adaptive changes in hearing. We discuss the mechanisms and maladaptive plasticity of NIHL, neuronal aspects of tinnitus triggers, and mechanisms such as tinnitus-associated neural changes at the cochlear nucleus underlying the generation of tinnitus after noise-induced deafferentation. We include observations from recent studies, including our own studies on associated risks and emerging treatments for tinnitus. Increasing knowledge of neural plasticity and adaptive changes in the central auditory system suggest that NIHL is preventable and transient abnormalities may be reversable, although ongoing research in assessment and early detection of hearing difficulties is still urgently needed. Since no treatment can yet reverse noise-related damage completely, preventative strategies and increased awareness of hearing health are essential. Full article
(This article belongs to the Special Issue Central Auditory Plasticity)
Review
Prepulse Inhibition of the Auditory Startle Reflex Assessment as a Hallmark of Brainstem Sensorimotor Gating Mechanisms
Brain Sci. 2020, 10(9), 639; https://doi.org/10.3390/brainsci10090639 - 16 Sep 2020
Cited by 6 | Viewed by 1096
Abstract
When a low-salience stimulus of any type of sensory modality—auditory, visual, tactile—immediately precedes an unexpected startle-like stimulus, such as the acoustic startle reflex, the startle motor reaction becomes less pronounced or is even abolished. This phenomenon is known as prepulse inhibition (PPI), and [...] Read more.
When a low-salience stimulus of any type of sensory modality—auditory, visual, tactile—immediately precedes an unexpected startle-like stimulus, such as the acoustic startle reflex, the startle motor reaction becomes less pronounced or is even abolished. This phenomenon is known as prepulse inhibition (PPI), and it provides a quantitative measure of central processing by filtering out irrelevant stimuli. As PPI implies plasticity of a reflex and is related to automatic or attentional processes, depending on the interstimulus intervals, this behavioral paradigm might be considered a potential marker of short- and long-term plasticity. Assessment of PPI is directly related to the examination of neural sensorimotor gating mechanisms, which are plastic-adaptive operations for preventing overstimulation and helping the brain to focus on a specific stimulus among other distracters. Despite their obvious importance in normal brain activity, little is known about the intimate physiology, circuitry, and neurochemistry of sensorimotor gating mechanisms. In this work, we extensively review the current literature focusing on studies that used state-of-the-art techniques to interrogate the neuroanatomy, connectomics, neurotransmitter-receptor functions, and sex-derived differences in the PPI process, and how we can harness it as biological marker in neurological and psychiatric pathology. Full article
(This article belongs to the Special Issue Central Auditory Plasticity)
Show Figures

Graphical abstract

Review
Silence, Solitude, and Serotonin: Neural Mechanisms Linking Hearing Loss and Social Isolation
Brain Sci. 2020, 10(6), 367; https://doi.org/10.3390/brainsci10060367 - 12 Jun 2020
Cited by 4 | Viewed by 1509
Abstract
For social animals that communicate acoustically, hearing loss and social isolation are factors that independently influence social behavior. In human subjects, hearing loss may also contribute to objective and subjective measures of social isolation. Although the behavioral relationship between hearing loss and social [...] Read more.
For social animals that communicate acoustically, hearing loss and social isolation are factors that independently influence social behavior. In human subjects, hearing loss may also contribute to objective and subjective measures of social isolation. Although the behavioral relationship between hearing loss and social isolation is evident, there is little understanding of their interdependence at the level of neural systems. Separate lines of research have shown that social isolation and hearing loss independently target the serotonergic system in the rodent brain. These two factors affect both presynaptic and postsynaptic measures of serotonergic anatomy and function, highlighting the sensitivity of serotonergic pathways to both types of insult. The effects of deficits in both acoustic and social inputs are seen not only within the auditory system, but also in other brain regions, suggesting relatively extensive effects of these deficits on serotonergic regulatory systems. Serotonin plays a much-studied role in depression and anxiety, and may also influence several aspects of auditory cognition, including auditory attention and understanding speech in challenging listening conditions. These commonalities suggest that serotonergic pathways are worthy of further exploration as potential intervening mechanisms between the related conditions of hearing loss and social isolation, and the affective and cognitive dysfunctions that follow. Full article
(This article belongs to the Special Issue Central Auditory Plasticity)
Show Figures

Graphical abstract

Review
Aging and Central Auditory Disinhibition: Is It a Reflection of Homeostatic Downregulation or Metabolic Vulnerability?
Brain Sci. 2019, 9(12), 351; https://doi.org/10.3390/brainsci9120351 - 01 Dec 2019
Cited by 4 | Viewed by 1319
Abstract
Aging-related changes have been identified at virtually every level of the central auditory system. One of the most common findings across these nuclei is a loss of synaptic inhibition with aging, which has been proposed to be at the heart of several aging-related [...] Read more.
Aging-related changes have been identified at virtually every level of the central auditory system. One of the most common findings across these nuclei is a loss of synaptic inhibition with aging, which has been proposed to be at the heart of several aging-related changes in auditory cognition, including diminished speech perception in complex environments and the presence of tinnitus. Some authors have speculated that downregulation of synaptic inhibition is a consequence of peripheral deafferentation and therefore is a homeostatic mechanism to restore excitatory/inhibitory balance. As such, disinhibition would represent a form of maladaptive plasticity. However, clinical data suggest that deafferentation-related disinhibition tends to occur primarily in the aged brain. Therefore, aging-related disinhibition may, in part, be related to the high metabolic demands of inhibitory neurons relative to their excitatory counterparts. These findings suggest that both deafferentation-related maladaptive plastic changes and aging-related metabolic factors combine to produce changes in central auditory function. Here, we explore the arguments that downregulation of inhibition may be due to homeostatic responses to diminished afferent input vs. metabolic vulnerability of inhibitory neurons in the aged brain. Understanding the relative importance of these mechanisms will be critical for the development of treatments for the underlying causes of aging-related central disinhibition. Full article
(This article belongs to the Special Issue Central Auditory Plasticity)
Show Figures

Figure 1

Back to TopTop