The hair cells of the inner ear are the functional sensory units of hearing and balance in the auditory and vestibular system, respectively, and are therefore a major cause of deafness and balance deficiencies when lost after damage. Unlike in reptiles, birds and fish, existing studies suggest that the mammalian sensory epithelia of the inner ear lack the ability to regenerate hair cells after such damage. Here we focus on the cristae, which are a component of the vestibular system, and are responsible for sensing angular acceleration and rotation of the head. Previous research has suggested that Notch activity, a crucial signaling pathway necessary for patterning the sensory epithelium, continues in adult mouse cristae, suggesting the potential for regeneration after damage. We characterized a lesion protocol for this system through the administration of the ototoxin iminodipropionitrile (IDPN) to test whether spontaneous regeneration of hair cells is present in the mammalian cristae. We used confocal microscopy to image the layers of the cristae's sensory epithelium after immunohistochemistry staining with markers specific to hair cells. Each cristae's hair cells were counted, and an average was obtained for cristae for each of several time points after IDPN injection. Preliminary findings show a severe reduction in total hair cell number in the mouse cristae one week after IDPN injection, and continued loss of hair cells in subsequent weeks. While we saw no evidence of spontaneous regeneration in the mouse cristae, this lesion protocol may be used in further hair cell regeneration studies using various manipulations or drugs, such as inhibition of Notch signaling.