Meeting Abstract
Ototoxicity is the harm induced on the cochlear or vestibular system of the ear that may lead to hearing loss and tinnitus. There is no current treatment for ototoxicity, yet there are over two hundred medications that result in hearing loss. The mode of action of these drugs is not clearly understood. This research seeks to determine the pathway used by the antibiotic, Gentamicin, to induce hearing loss. The model organism used is Nematostella vectensis, a sea anemone which possesses hair cells used in prey detection that are remarkably similar to the hair cells of human ears. Similarities include apical hair bundle mechanoreceptors composed of actin-based stereocilia and cadherin-based tip-links, and a loss of mechanotransduction with exposure to aminoglycoside antibiotics. To test the effects of Gentamicin on anemone hair cells, anemones were exposed to 1 mM Gentamicin dissolved in 12 ppt seawater for 4 hours then tentacles were excised and processed for microscopy. Phase-contrast and fluorescence microscopy were used to measure morphological features of the hair bundles, to obtain density of bundles and to obtain density of nuclei on the tentacles. Results show a significant decrease in the density of the Gentamicin-treated hair bundles compared to seawater controls, yet no significant change in the morphology of remaining hair bundles, or in the number of nuclei. Thus, Gentamicin has an acute effect leading to hair bundle loss but does not lead to immediate hair cell death. Ongoing experiments are aimed at testing the effects of Furosemide, a loop diuretic linked to ototoxicity. Considering the many similarities between hair cells in anemones and those in human inner ears, it is hoped that information gained in these experiments may indicate the mechanistic pathway of the drugs that lead to hearing loss.
