The sense of orientation in space is crucial for survival and navigation in the environment. The brain derives spatial orientation from (1) self-motion signals originating in the vestibular system of the inner ear and (2) visual signals encoding orientation relative to external landmarks. Previous studies in animal models have shown that spatial orientation is compromised after vestibular lesions, but the relationship between partial lesions and the degree of functional impairment has not been established.In the present study, navigation and spatial orientation capacities were tested in a modified version of the Oasis maze before and after the induction of graded vestibular lesions. Rats were water deprived and trained to collect water from only one of the 21 wells present in the maze. Prominent visual cues were provided to aid in the location of said well. Vestibular dysfunction was induced using sub-acute doses of the ototoxic agent 3,3'-iminodipropionitrile (IDPN) and was quantified using an anti-gravity reflex called tail-lift reflex. Afterwards, the vestibular epithelia were collected and processed via immunohistoch emistry to estimate the loss of hair cells (HCs).Initial results have shown that in a dose-dependent manner, vestibular toxicity caused a disrupted rat navigation in the Oasis maze, as indicated by an increase in movement, speed and time used to find the well. Current research aims to determine the correlation between the type and location of the HC loss and the degree of impairment in the Oasis maze spatial navigation task.Funded by PCI2020-120681-2, MCIN/AEI/ 10.13039/501100011033NextGenerationEU”/PRTR.