Meeting Abstract
Tentacles of sea anemones are covered with hair bundle mechanoreceptors that are employed to detect swimming movements of prey. Previously, sea anemones were exposed to calcium-depleted seawater in order to traumatize the hair bundles. This trauma disrupts linkages interconnecting stereocilia of the hair bundle. The linkages are necessary to maintain structural integrity of the hair bundle. This type of damage mimics that caused by large mechanical forces presumably experienced by the animal in nature. Due to the rapid recovery of anemone hair bundles following this type of trauma, however, it is thought that exposure to calcium-depleted seawater does not cause hair cell death. Is this resiliency of anemone hair bundles limited to restoring linkages? In the current study, we employed Cytochalasin D (CD), a fungal toxin that prevents actin polymerization, to damage the core of polymerized actin that forms the cytoskeleton within the stereocilia of anemone hair bundles. We determined the extent of damage caused to the hair bundles by evaluating hair bundle abundance, morphology, function, and relative F-actin content after CD trauma. We found that hair bundle abundance and function decrease with CD treatment, while morphology and relative F-actin content remain unchanged relative to controls. Hair bundle abundance returns to control levels within three hours. Although CD changes some aspects of vibration sensitivity in sea anemones, a base level of function remains. Taken together, these data confirm the resiliency of anemone hair cells.
