Washington, May 4 (ANI): A stress-response system within the cochlea mirrors the signaling pathways of the body”s fight or flight response, a study has shown for the first time.
Researchers have identified a hormone-like signaling system of the inner ear that sets baseline hearing sensitivity and helps protect against noise-induced hearing loss.
“Our research shows, for the first time, that the cochlea”s protective mechanism is likely to be largely a locally-produced phenomenon. The current theory of protection is that signals from the cochlea travel to the brain and back. While this theory does work under certain circumstances, we have known that it requires moderately-high intensity sounds to function. Our study demonstrates that a previously unrecognized signaling system involved in noise-induced hearing loss exists entirely within the ear. This signaling system works at lower intensity sounds – typical of our everyday environment – than the pathway involving the brain,” explained Doug Vetter, PhD, senior author and lecturer in the department of neuroscience at Tufts University School of Medicine.
“The local signaling system that we identified in the cochlea mirrors the molecular signaling pathways of the body”s physiological fight-or-flight response, which is triggered by the release of molecules from the adrenal glands during times of physical stress. It may be that activation of the cochlea”s protective mechanism from physical stress changes the way the cells of the inner ear respond to the next exposure. In this way, protection may be established based on previous exposures, and prior to the next exposure to potentially damaging sounds,” continued Vetter.
In the study, Vetter and colleagues focused on a specific receptor for corticotropin-releasing factor (CRF), a peptide that acts as a hormone and neurotransmitter. In the typical hormone signaling system served by CRF, the hypothalamus secretes CRF in response to stress and triggers the release of glucocorticoids, which are involved in the body”s immune and inflammatory responses. (ANI)