By Drs. Senthilvelan Manohar, Kelly Radziwon, and Richard Salvi
What do jet engines, sirens, and rock bands have in common? The sounds they emit are so intense that they are not only loud, but also painful, sometimes evoking a painful sensation around the external ear. The acoustic threshold for pain, 130-140 dB SPL, is intense enough to destroy or damage the delicate sensory hair cells, supporting cells and auditory nerve fibers in the inner ear. The axons from the auditory nerve deliver their messages to neurons located in the cochlear nuclei in the brainstem.
In a recent paper published in Molecular and Cellular Neuroscience, Drs. Baizer and Manohar at the University at Buffalo were surprised to find that intense noise exposures that destroyed the sensory hair cells in the rat inner ear led to a prolonged period of auditory nerve fiber degeneration in the cochlear nucleus in the brainstem (Bazier et al., Neuroscience 303 (2015) 299–311). Nerve fiber degeneration was still occurring 6-9 months post-exposure, nearly a third of the rat’s lifespan. In brain regions where the fibers were degenerating, there was robust upregulation of brain immune cells (microglia), indicative of long-term neuro-inflammation triggered by the release of inflammatory molecules in the brain. Since sensory nerve fibers (e.g., pain, touch) from the face, head, neck and shoulders (facial, trigeminal and spinal nerves) enter the cochlear nucleus, the long-term neuro-inflammation occurring in this region could lower pain thresholds (hyperalgesia). If this were to occur, much lower, moderate-intensity sounds (60-80 dB) might be sufficient to cause hyperacusis (loudness intolerance) with ear pain.
With funding from the Hearing Health Foundation obtained by Drs. Radziwon* and Manohar to identify pain-related molecules in the auditory pathway as a result of noise exposure, Drs. Manohar, Adler, and Salvi carried out a second study in which they measured noise-induced changes in the expression (amount) of genes involved in the synthesis of proteins known to be involved in neuropathic pain and neuro- inflammation. Interestingly, the researchers found that intense noise exposure significantly altered the expression of six genes (Ccl12, Tlr2, Oprd1, II1b, Ntrk1 & Kcnq3) in the cochlear nucleus (Manohar et al., Molecular and Cellular Neuroscience 75 (2016) 101–112). These results suggest that noise-induced inflammation in the parts of the central auditory pathway that also processes sensory information related to pain might, in turn, activate the central pain pathway thus producing ear pain. Determining whether neuro-inflammation is directly responsible for ear pain will open the door for novel interventions to treat hearing loss and hyperacusis.