Abstract

Noise exposure affects the organ of Corti and the lateral wall of the cochlea, including the stria vascularis and spiral ligament. Although the inner ear vasculature and spiral ligament fibrocytes in the lateral wall consist of a significant proportion of cells in the cochlea, relatively little is known regarding their functional significance. In this study, 6-week-old male C57BL/6 mice were exposed to noise trauma to induce transient hearing threshold shift (TTS) or permanent hearing threshold shift (PTS). Compared to mice with TTS, mice with PTS exhibited lower cochlear blood flow and lower vessel diameter in the stria vascularis, accompanied by reduced expression levels of genes involved in vasodilation and increased expression levels of genes related to vasoconstriction. Ultrastructural analyses by transmission electron microscopy revealed that the stria vascularis and spiral ligament fibrocytes were more damaged by PTS than by TTS. Moreover, mice with PTS expressed significantly higher levels of proinflammatory cytokines in the cochlea (e.g., IL-1β, IL-6, and TNF-α). Overall, our findings suggest that cochlear microcirculation and lateral wall pathologies are differentially modulated by the severity of acoustic trauma and are associated with changes in vasoactive factors and inflammatory responses in the cochlea.

Highlights

  • The World Health Organization estimates that 12% or more of the global population is at risk of hearing loss from noise, which impacts more than 600 million people worldwide [1,2,3]

  • Mice with transient hearing threshold shift (TTS) showed a gradual reduction in threshold shift, while those with permanent hearing threshold shift (PTS) maintained a high level of threshold shift until 14 days after noise exposure, which indicates that TTS mice recovered from noise trauma over time, whereas PTS mice did not

  • We evaluated how the cochlear lateral wall is affected by different noise conditions

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Summary

Introduction

The World Health Organization estimates that 12% or more of the global population is at risk of hearing loss from noise, which impacts more than 600 million people worldwide [1,2,3]. The major capillary systems in the spiral ligament and stria vascularis form four distinct networks (supra- and post-strial capillary networks of the spiral ligament, ad-strial capillary network of the spiral ligament, and capillaries of the stria vascularis) [14] which modulate cochlear endolymph homeostasis through generation of ionic gradients and K+ recycling between perilymph and endolymph [15]. These capillaries, play crucial roles in controlling sensory hair cell transduction by regulating endocochlear potential, ion transport, and endolymphatic fluid balance [16,17,18,19,20]. Dysfunction of the cochlear lateral wall is considered a potential etiology for a number of hearing disorders, including NIHL [10,21,22,23]

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