Vestibular compensation consists of the following stages: the inhibition of the contralesional medial vestibular nucleus (contra-MVe) activities at the acute stage after unilateral labyrinthectomy (UL) and the recovery and maintenance of the ipsilesional MVe (ipsi-MVe) spontaneous activities at the chronic stage after UL. In this paper, we reviewed molecular mechanisms of vestibular compensation in the central vestibular system by means of several morphological and pharmacological approaches in rats. Based on our examinations, we propose the following hypothesis. At the acute stage after UL, the activated neurons in the ipsi-MVe project their axons into the flocculus to inhibit the contra-MVe neurons via NMDA receptor, nitric oxide (NO), acetylcholine (Ach) and/or GABA-mediated signaling, resulting in the restoration of balance between intervestibular nuclear activities. At the chronic stage after UL, the flocculus depresses the inhibitory effects on the ipsi-MVe neurons via protein phosphatase 2A (PP2A) β, protein kinase C (PKC) and/or glutamate receptor (GluR) δ-2, to help the recovery and maintenance of the ipsi-MVe activities.
