Abstract
A lack of sleep is linked with a range of inner ear diseases, including hearing loss and tinnitus. Here, we used a mouse model to investigate the effects of sleep deprivation (SD) on noise vulnerability, and explored the mechanisms that might be involved in vitro, focusing particularly corticosterone levels and autophagic flux in cells. Female BALB/c mice were divided into six groups [control, acoustic trauma (AT)-alone, 1 day (d) SD-alone, 1d SD pre-AT, 5d SD-alone, and 5d SD pre-AT]. Cochlear damage was then assessed by analyzing auditory brainstem response (ABR), and by counting outer hair cells (OHCs) and the synaptic ribbons of inner hair cells (IHCs). In addition, we measured levels of serum corticosterone and autophagy protein expression in the basilar membranes by ELISA kits, and western blotting, respectively. We found that SD-alone temporarily elevated ABR wave I amplitude, but had no permanent effect on hearing level or IHC ribbon numbers. Combined with AT, the number of synaptic ribbons in the 1d SD pre-AT group was significantly higher than that in the AT-alone group, whereas the 5d SD pre-AT group showed more severe synaptopathy, and a greater loss of OHCs after 2 weeks than the other experimental groups exposed to noise. Correspondingly, the levels of corticosterone in the AT-alone group were higher than those of the 1d SD pre-AT group, but lower than those of the 5d SD pre-AT group. The 1d SD pre-AT group showed a marked elevation in the expression of microtubule-associated protein 1 light chain 3B (LC3B), whereas the AT-alone group exhibited only a mild increase. In contrast, the levels of LC3B did not change in the 5d SD pre-AT group. Experiments with HEI-OC-1 cells and cochlear basilar membrane cultures showed that high-concentrations of dexamethasone, and the inhibition of autophagy, aggravated cellular apoptosis induced by oxidative stress. In conclusion, noise-induced synaptopathy and hair cell loss can be mitigated by preceding 1d SD, but will be aggravated by preceding 5d SD. These findings may be attributable to corticosterone levels and the extent of autophagy.
Highlights
Sleep is indispensable for the homeostasis of organisms, and is closely associated with circadian rhythms (Goel et al, 2013) and hormone levels (Mônico-Neto et al, 2015)
After 2 weeks, the auditory brainstem response (ABR) wave I amplitudes of the standard deviation (SD) groups reduced to levels that were equivalent to the control group
We used a mouse model to demonstrate that noise-induced synaptopathy varied with the duration of sleep deprivation (SD), and that the noise-induced hearing threshold shift did not change with the duration of SD
Summary
Sleep is indispensable for the homeostasis of organisms, and is closely associated with circadian rhythms (Goel et al, 2013) and hormone levels (Mônico-Neto et al, 2015). The number of people suffering from sleep disorders is increasing, those who only sleep for a few hours each night (Foster and Kreitzman, 2014). Over 50% of sudden deafness patients had previously experienced SD (Yang et al, 2015). From another aspect, both animal and human studies have demonstrated that noise could alter the auditory brainstem response (ABR) and produce tinnitus without affecting the function of the outer hair cells (Bramhall et al, 2017; Liberman and Kujawa, 2017). Studies have reported an increased risk of tinnitus in humans when there was a reduction in the wave I amplitude of ABR (Bramhall et al, 2018). Whether SD alone causes cochlear injury, or whether SD modifies susceptibility to noise, has yet to be elucidated
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