THE INTRINSIC-PROPERTIES OF VESTIBULAR NUCLEUS NEURONS AND RECOVERY OF MOTOR FUNCTION FOLLOWING PERIPHERAL VESTIBULAR DEAFFERENTATION - IS THERE A LINK

Unilateral labyrinthectomy (UL) induces a syndrome of eye movement and postural disorders which disappears over time in a process of behavioural recovery known as vestibular compensation. Vestibular compensation is associated with a partial regeneration of resting activity in neurons in the vestibular nuclei (VN) on the side of UL. Two recent lines of evidence suggest (1) that intrinsic properties (e.g. persistent ion conductances) of VN neurons may contribute to this neuronal recovery and (2) that intracellular calcium (Ca2+) may be important in vestibular compensation. The 'intrinsic mechanism' hypothesis is consistent with the demonstration that VN neurons have the capacity to generate resting activity in vitro, in the absence of normal synaptic input. Recent studies suggest that systemic treatment with Ca2+ channel antagonists such as flunarizine and verapamil may facilitate vestibular compensation. It is possible that Ca2+ antagonists limit an excessive Ca2+ influx at the time of UL and thereby facilitate the regeneration of resting activity which is responsible for vestibular compensation.