In response to chronic stress, mammalian vestibular hair cells (HC) may undergo extrusion from the sensory epithelium. Before HC loss begins, the early damage is characterized by synaptic uncoupling and dismantlement of the calyceal junction, the cell adhesion complex formed between type I HCs and calyx afferents. This early pathology associates with the early loss of vestibular function, and both the initial epithelial and functional alterations are reversible. This study was aimed at identifying key gene expression responses associated with these phenomena. We used three animal models of chronic ototoxicity at similar stages of loss of vestibular reflexes: mice and rats exposed to 3,3'-iminodipropionitrile and rats exposed to streptomycin. Shorter and longer exposure times of the rat IDPN model were also assessed. Vestibular sensory epithelia were collected and processed by RNA-seq, so 5 datasets of differentially expressed genes (DEG) between treated and control groups (n=3/group) were obtained. Comparing the resulting lists, we identified 32 genes downregulated in common in all five treated vs. control comparisons. Among these, 24 have been identified to be specifically expressed by HCs (Bdnf, Bmp2, Ntrk3, Xirp2, Ptprq and others), with no information available for the cell-type specificity of the other 8. By immunohistochemistry and confocal microscopy, we observed decreased expression of the proteins encoded by some of these HC-specific genes (PMCA2/Atp2b2, DNER/Dner, Kv1.8/KCNA10). We conclude that vestibular HCs under chronic ototoxic stress downregulate the expression of genes that characterize their mature functional phenotype. Funded by PID2021-124678OB-I00/ AEI/10.13039/501100011033/ FEDER, UE.