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Whole membranous labyrinths of bullfrogs were used in order to replicate the human vestibule. The posterior semicircular canals (PSCs) were exposed, leaving the remaining membranous labyrinth encapsulated in the otic capsule. Vibration was applied to the surface of the bony capsule using a conventional surgical drill in order to dislodge the otoconia from the utricle. The position of the preparation was controlled so that the dislodged otoconia were attached to the cupular surface. This was regarded as a cupulolithiasis model. The action potentials changed instantaneously according to the gravitational force on the cupula. When the otoconia were dislodged and held within the PSC lumen, the position of the whole preparation was changed so that the otoconia moved back and forth within the canal lumen. This is a model of canalolithiasis. The action potentials changed in combination with the otoconial movement after a latent period. Both cupulolithiasis and canalolithasis are potentially valid mechanisms of benign paroxysmal positional vertigo (BPPV). However, canalolithiasis is the most likely mechanism of BPPV, which is usually characterized by nystagmus of short duration and long latency. A vibratory stimulus was able to detach the otoconia from the utricle, suggesting that mechanical insult could be a possible etiology of BPPV.