Vestibular compensation modifies the sensitivity of vestibular neurones to inhibitory amino acids.

The progressive disappearance of the postural and oculomotor syndrome triggered by unilateral labyrinthectomy (vestibular compensation) is a model of plasticity in the adult central nervous system. This recovery may involve modifications of the pharmacological profile of central vestibular neurones, in particular their sensitivity to inhibitory amino acids. We therefore compared the sensitivity of medial vestibular nucleus neurones to glycine and muscimol in slices taken either from control animals, or from guinea-pigs labyrinthectomized 3 days before. We demonstrate that the loss of excitatory inputs experienced by the ipsilesional vestibular neurones induces a decrease in their sensitivity to inhibitory amino acids. These pharmacological changes should facilitate the recovery of a normal balance between the average resting discharge of neurones in both vestibular nuclei.