<p>The vestibular organs of birds are capable of regenerating sensory hair cells after ototoxic injury, but the regenerative ability of the mammalian vestibular organs is much more limited. The factors that inhibit regeneration in the mammalian inner ear are not known, but it has been proposed that the structure of filamentous actin cables at cell–cell junctions may be an important regulatory influence. Junctional actin cables in the chick utricle are relatively thin, while those in the&#xa0;mouse utricle are much thicker. These differences result in differing mechanical properties of the avian vs. mammalian inner ear, which may affect the potential for regenerative proliferation. In the present study, I characterized injury-evoked changes in junctional actin cables and supporting cell surface areas in the utricles of mice and chicks of either sex. I found that the thickness of junctional cables in the chick utricle was not affected by ototoxic injury, but that injury to the mouse utricle resulted in the formation of numerous new junctional actin bands whose thickness was comparable to those in the chick utricle. Thicker actin bands also persisted after injury, but were not necessarily associated with cellular junctions. I further found that moderate hair cell injury caused supporting cells in the chick utricle to expand their lumenal surfaces by about 50%, while comparable injury to the mouse utricle caused supporting cells to expand by only ~ 30%. I speculate that this difference may impact the injury-induced activation of Hippo/YAP signaling.</p>