A recent study has found that high noise levels result in the upregulation of genes responsible for inflammation and pain in the cochlear nucleus (low level auditory brain). The study was performed at the University of Buffalo and is an indirect product of the lobbying of Hyperacusis Research. One of this paper’s authors, Dr. Salvi, is a scientific advisor at Hyperacusis Research. Donate to Hyperacusis Research to help fund more studies like these.
“In the pain and inflammatory array, noise exposure upregulated mRNA expression levels of four pain/inflammatory genes, Tlr2, Oprd1, Kcnq3 and Ntrk1 and decreased mRNA expression levels of two more genes, Ccl12 and Il1β. Pain/inflammatory gene expression changes via Ntrk1 signaling may induce sterile inflammation, neuropathic pain, microglial activation and migration of nerve fibers from the trigeminal, cuneate and vestibular nuclei into the CN. These changes could contribute to somatic tinnitus, hyperacusis and otalgia.”