Role of glucocorticoid in vestibular compensation in relation to activation of vestibular nucleus neurons.

It is still not established whether or not glucocorticoids are effective in the treatment of vestibular disorders such as dizziness and imbalance, although these drugs in combination with several others are used to treat dizziness and imbalance in some diseases. This study was undertaken to investigate the effects of a glucocorticoid, dexamethasone, on vestibular disorder following unilateral labyrinthectomy in pigmented rabbits. Neuronal activities of the medial vestibular nucleus (MVN) in alpha-chloralose-anesthetized cats were also investigated. Systemic injection of dexamethasone decreased the frequency of nystagmus and head deviation dose-dependently following hemilabyrinthectomy, and the rate of decrease was faster than that obtained by saline. In contrast, RU38486 (a glucocorticoid receptor antagonist) delayed the reduction of nystagmus and head deviation. Micro-iontophoretic application of dexamethasone rapidly enhanced the spontaneous firing of MVN neurons in a dose-dependent manner. These increases were blocked by RU38486, but not by GDEE (a glutamate receptor antagonist) or Co2+ (a Ca2+ channel blocker). These results suggest that dexamethasone directly activates the MVN neurons, thereby accelerating vestibular compensation.