Genetics of age-related hearing loss in mice. III. Susceptibility of inbred and F1 hybrid strains to noise-induced hearing loss

1996 ◽  
Vol 93 (1-2) ◽  
pp. 181-187 ◽  
Author(s):  
Lawrence C. Erway ◽  
Yea-Wen Shiau ◽  
Rickie R. Davis ◽  
Edward F. Krieg
1993 ◽  
Vol 65 (1-2) ◽  
pp. 125-132 ◽  
Author(s):  
Lawrence C. Erway ◽  
James F. Willott ◽  
Jonathan R. Archer ◽  
David E. Harrison

2018 ◽  
Author(s):  
Daniel Lyngholm ◽  
Shuzo Sakata

AbstractWith the advent of recent genetic technologies for mice, it is now feasible to investigate the circuit mechanisms of brain functions in an unprecedented manner. Although transgenic mice are commonly used on C57BL/6J (C57) background, hearing research has typically relied on different genetic backgrounds, such as CBA/Ca or CBA due to the genetic defect of C57 mice for early age-related hearing loss. This limits the utilization of available genetic resources for hearing research. Here we report congenic (>F10) Cre-dependent channelrhodopsin2 (ChR2) mice on CBA/Ca background. By crossing this line with Cre-driver mice on C57 background, F1 hybrids restored the hearing deficit of C57 mice. We also found a linear relationship between aging and hearing loss, with progression rates varied depending on genetic backgrounds (3.39 dB/month for C57; 0.82 dB/month for F1 hybrid). We further demonstrate that this approach allows to express ChR2 in a specific type of inhibitory neurons in the auditory cortex and that they can be identified within a simultaneously recorded population of neurons in awake mice. Thus, our Cre-dependent optogenetic transgenic mice on CBA/Ca background are a valuable tool to investigate the circuit mechanisms of hearing across lifespan.


2020 ◽  
Author(s):  
Fan Ye ◽  
Bi Lin ◽  
Lian Fang

Abstract Noise induced hearing loss (NIHL) is a kind of hearing impairment, which is next to the age-related hearing loss. More and more evidences have verified that overproduction of reactive oxygen species is a common pathologic phenomenon of different inner ear injury including NIHL, and autophagy contributes to attenuate NIHL by reducing oxidative stress. However, the underlying mechanism by which noise exposure causes autophagy activation remains unclear. In this study, we found that NIHL was accompanied by autophagy in the rat cochlea. Furthermore, twelve common genes were found at the GEO datasets GSE85290 and GSE8342, and E3 ubiquitination ligase FBXO3 was confirmed significantly reduced in NIHL rat cochlea. Next, we demonstrated that FBXO3 can directly binding with autophagy-related protein 10 (ATG10), which is necessary for the initiation of autophagy, and mediate its degradation. In vivo animal model treatment with rapamycin, an autophagy activator, significantly reduced the NIHL. Based on these data, we confirmed that FBXO3 played an important role in autophagy caused by NIHL, may be a potential target of NIHL treatment.


1995 ◽  
Vol 112 (5) ◽  
pp. P75-P75
Author(s):  
Robert A. Dobie

Educational objectives: To understand the epidemiology of noise-induced hearing loss (NIHL) and age-related hearing loss (ARHL), including time course, interactions, and importance of occupational and nonoccupational exposure history; to use clinical and epidemiologic data and principles to diagnose NIHL and ARHL; and to estimate the relative contributions of each in individual cases.


Author(s):  
Ruili Xie ◽  
Tessa-Jonne F. Ropp ◽  
Michael R. Kasten ◽  
Paul B. Manis

Hearing loss generally occurs in the auditory periphery but leads to changes in the central auditory system. Noise-induced hearing loss (NIHL) and age-related hearing loss (ARHL) affect neurons in the ventral cochlear nucleus (VCN) at both the cellular and systems levels. In response to a decrease in auditory nerve activity associated with hearing loss, the large synaptic endings of the auditory nerve, the endbulbs of Held, undergo simplification of their structure and the volume of the postsynaptic bushy neurons decreases. A major functional change shared by NIHL and ARHL is the development of asynchronous transmitter release at endbulb synapses during periods of high afferent firing. Compensatory adjustements in transmitter release, including changes in release probability and quantal content, have also been reported. The excitability of the bushy cells undergoes subtle changes in the long-term, although short-term, reversible changes in excitability may also occur. These changes are not consistently observed across all models of hearing loss, suggesting that the time course of hearing loss, and potential developmental effects, may influence endbulb transmission in multiple ways. NIHL can alter the representation of the loudness of tonal stimuli by VCN neurons and is accompanied by changes in spontaneous activity in VCN neurons. However, little is known about the representation of more complex stimuli. The relationship between mechanistic changes in VCN neurons with noise-induced or age-related hearing loss, the accompanying change in sensory coding, and the reversibility of changes with the reintroduction of auditory nerve activity are areas that deserve further thoughtful exploration.


Author(s):  
Rogan Corbridge ◽  
Nicholas Steventon

Conditions affecting the inner ear are delineated. Sensorineural hearing loss and its aetiologies are explored in reference to age-related hearing loss, noise-induced hearing loss, syndromic problems, and auditory neuropathy spectrum disorder. Causes of vertigo related to peripheral vestibular dysfunction are discussed, including vestibular migraine. Management of temporal bone fractures and their sequelae are explored. Methods of hearing rehabilitation are described.


2016 ◽  
Vol 17 (2) ◽  
pp. 68-73
Author(s):  
Dong-Wook Kim ◽  
Tae-Young Lee ◽  
Da-Hye Choi ◽  
Taek-Yeong Kim ◽  
Hyun-Chul Moon

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