Abstract
BackgroundNoise exposure (NE) is a severe modern health hazard that induces hearing impairment. However, the noise-induced ultrastructural changes of blood-labyrinth barrier (BLB) and the potential involvements of tight junction proteins (TJP) remain inconclusive.We investigated the effects of NE on not only the ultrastructure of cochlea and permeability of BLB but also the expression of TJP within the guinea pig cochlea.ResultsMale albino guinea pigs were exposed to white noise for 4 h or 2 consecutive days (115 dB sound pressure level, 6 hours per day) and the hearing impairments and light microscopic change of BLB were evaluated with auditory brainstem responses (ABR) and the cochlear sensory epithelia surface preparation, respectively. The cochlear ultrastructure and BLB permeability after NE 2d were revealed with transmission electron microscope (TEM) and lanthanum nitrate-tracing techniques, respectively. The potential alterations of TJPs Claudin-5 and Occludin were quantified with immunohistochemistry and western blot. NE induced significant hearing impairment and NE 2d contributed to significant outer hair cell (OHC) loss that is most severe in the first row of outer hair cells. Furthermore, the loosen TJ and an obvious leakage of lanthanum nitrate particles beneath the basal lamina were revealed with TEM. Moreover, a dose-dependent decrease of Claudin-5 and Occludin was observed in the cochlea after NE.ConclusionsAll these findings suggest that both decrease of Claudin-5 and Occludin and increased BLB permeability are involved in the pathologic process of noise-induced hearing impairment; however, the causal relationship and underlying mechanisms should be further investigated.Electronic supplementary materialThe online version of this article (doi:10.1186/s12868-014-0136-0) contains supplementary material, which is available to authorized users.
Highlights
Noise exposure (NE) is a severe modern health hazard that induces hearing impairment
The alteration of blood-labyrinth barrier (BLB) permeability caused by NE has become the research focus because the integrity of BLB plays a crucial role in stabilizing cochlear microenvironment and maintaining the function of inner ear [7,8]
There was no loss of outer hair cell (OHC) in the control (Figure 1A, Ctrl) cochlear sample, few OHC loss in the NE 4 h sample (Figure 1A, NE 4 h) but severe loss of OHC in the NE 2d sample (Figure 1A, NE 2 h)
Summary
Noise exposure (NE) is a severe modern health hazard that induces hearing impairment. Hearing impairment occurs in many noise exposure (NE) environments, including occupational (e.g., industrial, military), or recreational (e.g., musical concerts, hunting) settings and is closely related with the underlying cochlear pathologies including the increased endocytosis, vacuolation, mitochondrial lesion, elevated intracellular Ca2+ concentration and the generation of reactive oxygen. Among these pathological changes, the alteration of BLB permeability caused by NE has become the research focus because the integrity of BLB plays a crucial role in stabilizing cochlear microenvironment and maintaining the function of inner ear [7,8]. Alteration of TJs can significantly affect the BLB permeability
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