Transient receptor potential vanilloid-1 (TRPV1) is a mediator of noise-induced neural damage in zebrafish and mice.

Abstract

Sound pollution (noise) is an increasing environmental concern, particularly associated with neurological and neurobehavioral abnormalities. However, the molecular mechanisms underlying noise-induced neural damage remain unclear. In this study, we conducted transcriptional profiling of zebrafish to investigate the mechanisms underlying acoustic stimulation (1,000 Hz, 130 dB). RNA sequencing and subsequent experiments revealed that TRPV1 is an important mediator of noise-induced neural damage in HuC(elavl3)-GFP transgenic zebrafish. The results demonstrated that inhibiting TRPV1 significantly mitigated noise-induced neural damage in zebrafish with trpv1 gene RNAi and in mice with Trpv1 knockout (Trpv1^-/-). Specifically, TRPV1 antagonism significantly reduced neural damage in zebrafish and mice under noise exposure. Furthermore, activated TRPV1 could induce endoplasmic reticulum stress, leading to apoptosis and resulting in neural damage in mice and HEK293T cells. The findings of this study not only enhance our understanding of the molecular mechanisms underlying sound-induced neural damage but also highlight a novel target for drug intervention.