How endolymph pressure modulates semicircular canal primary afferent discharge.

Histological observation of endolymphatic hydrops in subjects suffering from Meniere's disease/syndrome and the presence of vestibular symptoms in experimentally induced endolymphatic hydrops have led to considerable debate regarding the potential role of inner-ear pressure. Could a condition influencing endolymphatic volume regulation lead to transient changes in translabyrinthine pressure sufficiently large to alter primary afferent discharge rates? To investigate this question we built a highly sensitive laser-based pressure sensor and recorded endolymphatic pressure modulations within the horizontal semicircular canal ampulla in response to mechanical stimuli for simple head rotation and controlled volume injection. The most sensitive primary afferents responded to changes in endolymph pressures as low as 0.005 Pa (re: perilymph)--a pressure considerably lower than that observed in most experimentally induced hydropic conditions. This threshold pressure was generated by a approximately 25 picoliter volume injection stimulus. Semicircular canal afferent responses to endolymphatic pressure can be explained on the basis of pressure-induced hydrops, which causes dilation of the ampulla, deformation of the cupula, hair bundle movement, and afferent discharge. Primary afferent responses to maintained stimuli were transient in nature and recovered to pre-stimulus background discharge rates following a period of adaptation. Results demonstrate that the semicircular canals are indeed sensitive to small changes in translabyrinthine pressure in addition to head-movement-related changes in transcupular pressure.