scholarly journals Roles of Key Ion Channels and Transport Proteins in Age-Related Hearing Loss

2021 ◽  
Vol 22 (11) ◽  
pp. 6158
Author(s):  
Parveen Bazard ◽  
Robert D. Frisina ◽  
Alejandro A. Acosta ◽  
Sneha Dasgupta ◽  
Mark A. Bauer ◽  
...  

The auditory system is a fascinating sensory organ that overall, converts sound signals to electrical signals of the nervous system. Initially, sound energy is converted to mechanical energy via amplification processes in the middle ear, followed by transduction of mechanical movements of the oval window into electrochemical signals in the cochlear hair cells, and finally, neural signals travel to the central auditory system, via the auditory division of the 8th cranial nerve. The majority of people above 60 years have some form of age-related hearing loss, also known as presbycusis. However, the biological mechanisms of presbycusis are complex and not yet fully delineated. In the present article, we highlight ion channels and transport proteins, which are integral for the proper functioning of the auditory system, facilitating the diffusion of various ions across auditory structures for signal transduction and processing. Like most other physiological systems, hearing abilities decline with age, hence, it is imperative to fully understand inner ear aging changes, so ion channel functions should be further investigated in the aging cochlea. In this review article, we discuss key various ion channels in the auditory system and how their functions change with age. Understanding the roles of ion channels in auditory processing could enhance the development of potential biotherapies for age-related hearing loss.

2013 ◽  
Vol 22 (2) ◽  
pp. 299-302 ◽  
Author(s):  
Robert D. Frisina ◽  
D. Robert Frisina

Purpose The aim of this study was to highlight growing evidence of interactions between hormones and the structure and function of the auditory system. Method Recent studies implicating sex hormones and other natural hormones in the modulation of hearing status in age-related hearing loss were reviewed. Results Progesterone, a sex hormone, has been shown to have negative effects on the hearing of older women and aging mice, whereas, in contrast, estrogen was found in some cases to have a positive influence. Aldosterone, used in studies of animal models of autoimmune hearing loss, slowed the progression of hearing loss. Follow-up studies in humans revealed that auditory measures varied as serum aldosterone levels shifted within the normal range, in otherwise healthy older subjects. This was true for simple as well as complex auditory tasks (i.e., sound spatial processing), suggesting benefits of aldosterone to postperipheral auditory processing as well. In addition, evidence suggests that this functional hearing improvement occurred in association with anatomical improvements to the stria vascularis—an important site of anatomical change in presbycusis. Conclusions Audiology is now at the point where the search for biomedical interventions to modulate or prevent age-related hearing loss can move forward. Such interventions would require multidisciplinary collaborative initiatives by researchers in such areas as drug development, anatomy, auditory physiological and perceptual testing, and drug microdelivery systems.


Author(s):  
Donald M. Caspary ◽  
Daniel A. Llano

As arguably the third most common malady of industrialized populations, age-related hearing loss is associated with social isolation and depression in a subset of the population that will approach 25% by 2050. Development of behavioral or pharmacotherapeutic approaches to prevent or delay the onset of age-related hearing loss and mitigate the impact of hearing loss of speech understanding requires a better understanding of age-related changes that occur in the central auditory processor. This chapter critically reviews and discusses changes that occur in the auditory brainstem and thalamus with increased age. It briefly discusses age-related cellular changes that occur de novo within the central auditory system versus deafferentation plasticity and animal models of aging. Subsections discuss the cochlear nucleus, superior olivary complex, inferior colliculus, and the medial geniculate body with an emphasis on age-related changes in neurotransmission and how these changes could underpin the observed loss of precise temporal processing with increased age.


2020 ◽  
Author(s):  
Meijian Wang ◽  
Chuangeng Zhang ◽  
Shengyin Lin ◽  
Yong Wang ◽  
Benjamin J. Seicol ◽  
...  

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.


2018 ◽  
Vol 29 (01) ◽  
pp. 005-014 ◽  
Author(s):  
Cristina F. B. Murphy ◽  
Camila M. Rabelo ◽  
Marcela L. Silagi ◽  
Leticia L. Mansur ◽  
Doris E. Bamiou ◽  
...  

AbstractDespite the well-established relationship between aging and auditory processing decline, identifying the extent to which age effect is the main factor on auditory processing performance remains a great challenge due to the co-occurrence of age-related hearing loss and age-related cognitive decline as potential confounding factors.To investigate the effects of age-related hearing loss and working memory on the clinical evaluation of auditory processing of middle-aged and elderly.Cross-sectional study.A total of 77 adults between 50 and 70 yr of age were invited to participate in the study.The participants were recruited from a larger study that focused on the assessment and management of sensory and cognitive skills in elderly participants. Only participants with normal hearing or mild-to-moderate age-related hearing loss, with no evidence of cognitive, psychological, or neurological conditions were included. Speech-in-noise, dichotic digit, and frequency pattern tests were conducted as well as a working memory test. The hearing loss effect was investigated using an audibility index, calculated from the audiometric threshold. The performance on the digit span test was used to investigate working memory effects. Both hearing loss and working memory effects were investigated via correlation and regression analyses, partialling out age effects. The significance level was set at p < 0.05.The results demonstrated that, while hearing loss was associated to the speech-in-noise performance, working memory was associated to the frequency pattern and dichotic digit performances. Regression analyses confirmed the relative contribution of hearing loss to the variance in speech-in-noise and working memory test to the variance in frequency pattern and dichotic digit test performance.The performance decline of the elderly in auditory processing tests may be partially attributable to the working memory performance and, consequently, to the cognitive decline exhibited by this population. Mild-to-moderate hearing loss seems to affect performance on specific auditory processing tasks, such as speech in noise, reinforcing the idea that auditory processing disorder in the elderly might also be associated to auditory peripheral deficits.


2018 ◽  
Vol 38 (13) ◽  
pp. 3177-3189 ◽  
Author(s):  
Teerawat Wiwatpanit ◽  
Natalie N. Remis ◽  
Aisha Ahmad ◽  
Yingjie Zhou ◽  
John C. Clancy ◽  
...  

2016 ◽  
Vol 116 (6) ◽  
pp. 2695-2705 ◽  
Author(s):  
Ruili Xie

Age-related hearing loss (ARHL) is largely attributed to structural changes and functional declines in the peripheral auditory system, which include synaptopathy at the inner hair cell/spiral ganglion cell (SGC) connection and the loss of SGCs. However, functional changes at the central terminals of SGCs, namely the auditory nerve synapses in the cochlear nucleus, are not yet fully understood during ARHL. With the use of young (1–3 mo) and old (25–30 mo) CBA/CaJ mice, this study evaluated the intrinsic properties of the bushy neurons postsynaptic to the endbulb of Held synapses, and the firing properties of these neurons to direct current injections as well as to synaptic inputs from the auditory nerve. Results showed that bushy neurons in old mice are more excitable and are able to fire spikes at similar rate and timing to direct current injections as those in young mice. In response to synaptic inputs, however, bushy neurons from old mice fired spikes with significantly decreased rate and reduced temporal precision to stimulus trains at 100 and 400 Hz, with the drop in firing probability more profound at 400 Hz. It suggests that transmission of auditory information at the endbulb is declined in both rate and timing during aging, which signifies the loss of sensory inputs to the central auditory system under ARHL. The study proposes that, in addition to damages at the peripheral terminals of SGCs as well as the loss of SGCs, functional decline at the central terminals of surviving SGCs is also an essential component of ARHL.


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