Acoustic Trauma Modulates Cochlear Blood Flow and Vasoactive Factors in a Rodent Model of Noise-Induced Hearing Loss

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.

The mechanoelectrical transducer channel is not required for regulation of cochlear blood flow during loud sound exposure in mice

“…The two control mechanisms, which are based in different vascular areas -lateral wall and arteriolar-possibly dominate at lower and higher SPLs respectively. This theory fits with the finding that both partial oxygen pressure 49 , and cochlear blood flow measured by LDF both acutely 16 and chronically 50 show such a relationship to sound intensity, and may partially contribute toward setting the sound level threshold above which the risk of hearing loss is significant.…”

Mitochondrial Damage and Necroptosis in Aging Cochlea

“…Samples from mice aged 2 and 20 months were collected. Cochlear tissues were obtained to localize inner and outer hair cells and neuronal fibers as previously described [20,21]. Briefly, tissues were fixed in 4% paraformaldehyde in phosphate-buffered saline (PBS) for 1 h at room temperature to remove the cochlear bony walls and lateral wall tissues and separated individual cochlear turns.…”

Adenosine A2B receptor: A pathogenic factor and a therapeutic target for sensorineural hearing loss

“…5 ADORA2A, on the contrary, is mainly expressed in the organ of Corti, spiral ganglion neurons (SGN), and cochlear vasculature and may play a detrimental role in HL by persistent vasodilation. 5,15 Among four adenosine receptors, ADORA2B has the least affinity for adenosine and is, therefore, only activated by chronically elevated levels of adenosine. Early studies showed that excess adenosine signaling via ADORA2B leads to multiple pathologies that induce disease progression, including chronic kidney disease, sickle cell disease, priapism, and preeclampsia.…”