AI Article Synopsis
- The study investigated the role of EP4 receptors in hearing, finding that mice lacking EP4 had hearing loss and reduced otoacoustic emissions due to outer hair cell loss.
- When exposed to loud noise, these EP4-deficient mice experienced greater auditory response shifts and OHC damage compared to normal mice.
- Activating EP4 helped protect OHCs from noise damage and reduced hearing loss, suggesting that EP4 could be a therapeutic target for cochlear diseases.
Article Abstract
This study explored the physiological roles of PGE-type receptor 4 (EP4) in auditory function. EP4-deficient mice exhibited slight hearing loss and a reduction of distortion-product otoacoustic emissions (DPOAEs) with loss of outer hair cells (OHCs) in cochleae. After exposure to intense noise, these mice showed significantly larger threshold shifts of auditory brain-stem responses (ABRs) and greater reductions of DPOAEs than wild-type mice. A significant increase of OHC loss was confirmed morphologically in the cochleae of EP4-deficient mice. Pharmacological inhibition of EP4 had a similar effect to genetic deletion, causing loss of both hearing and OHCs in C57BL/6 mice, indicating a critical role for EP4 signaling in the maintenance of auditory function. Pharmacological activation of EP4 significantly protected OHCs against noise trauma, and attenuated noise-induced hearing loss in C57BL/6 mice. These findings suggest that EP4 signaling is necessary for the maintenance of cochlear physiological function and for cochlear protection against noise-induced damage, in particular OHCs. EP4 might therefore be an effective target for cochlear disease therapeutics.
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| http://dx.doi.org/10.1016/j.neuropharm.2011.12.007 | DOI Listing |
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