Betahistine reduces the resting firing rate of vestibular receptors in the frog.
Although betahistine is widely used in the treatment of vertigo, it remains unclear whether it directly affects the vestibular system at the peripheral level. The effects of betahistine were therefore assessed in an isolated preparation of frog semicircular canal. Betahistine was administered either in the endolymphatic or the perilymphatic fluid and the ampullar receptor potential and mass nerve discharge were recorded at rest and during mechanical stimulation. Endolymphatic administration was without effect. In contrast, perilymphatic administration resulted in a marked reduction in ampullar receptor resting discharge, although the mechanically evoked responses were only slightly affected. As vertigo is generally caused by sudden and uncontrolled changes in the resting discharge of vestibular receptors, the ability of betahistine to reduce the resting firing rate of vestibular receptors is thought to contribute to its anti-vertigo actions.