Role of Glucocorticoid in Vestibular Compensation in Relation to Activation of Vestibular Nucleus Neurons

Section: Introductionmentioning

confidence: 57%

Immunocytochemical and stereological study of glucocorticoid receptors in rat medial vestibular nucleus neurons and the effects of unilateral vestibular deafferentation

Zhang

Smith

Darlington

2005

“…The secretion of corticosterone is known to increase under conditions of stress through the HPA axis (18,19), and the resulting increase in concentration of corticosterone inhibits adrenocorticotropic hormone (ACTH) secretion via a feedback system (19). Although ACTH has been reported to accelerate vestibular compensation (2), corticosterone may have various effects on vestibular compensation depending on its concentration; the effects of corticosterone through glucocorticoid receptors are fundamentally necessary for vestibular compensation (20,21), while overexposure to corticosterone attenuates postsynaptic excitability and cytotoxic effects through glucocorticoid receptors (22). In this study, the delay in vestibular compensation under conditions of stress may thus have been due to excess corticosterone and decrease in ACTH.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Stress Application on Vestibular Compensation

Yamamoto

Yamanaka²,

Matsunaga³

2000

It is still unknown how stress, which is known to delay recovery from vestibular symptoms in patients with vertigo, influences recovery from vertigo. We therefore investigated the effect of stress on vestibular compensation following unilateral labyrinthectomy (UL) as a model of recovery from vertigo. In addition, we examined the effect of trilostane (4alpha, 5-epoxy-17beta-hydroxy-3-oxo-5alpha-androstane-2alpha-carbon itrile; TRIL), an inhibitor of the steroid biosynthesis enzyme delta5-3beta-hydroxysteroid dehydrogenase (3beta-HSD), on vestibular compensation under conditions of stress. After UL, Wistar rats were divided into five groups as follows and subjected to stress and/or drug application: UL only (native, n = 6); UL + stress (S, n = 6); UL + vehicle (V, n = 5); UL + stress + vehicle (S + V, n = 5); and UL + stress + TRIL (S + TRIL, n = 5). In the S group, the decrease in frequency of spontaneous nystagmus (SN) was significantly (p < 0.05) slower than, in the native group at 3, 12, 24, 30, 36 and 48 h. The decreases in frequency of SN in the V and S + V groups were similar to those in the native and S groups, respectively, suggesting that neither handling on injection nor administration of vehicle affected vestibular compensation. In the S + TRIL group, the frequency of SN was significantly (p < 0.05) less than that m the S + V group at 24 h after UL. At 30 h, the frequency of SN m the S + TRIL group was almost the same as that in the V group. These findings suggest that stress attenuates vestibular compensation and that changes in steroid concentrations account at least in part for this attenuation.

“…Steroids are also used for the treatment of Meniere's disease and vestibular neuronitis (32,33). The first behavioural study investigating the effects of glucocorticoids on vestibular compensation in animals was not published until 1995 (34). Dexamethasone dose-dependently (1 or 5 mg/kg i.v., twice daily) accelerated the rate of spontaneous nystagmus and longitudinal head twist compensation, compared to saline-treated rabbits (34).…”

Section: Experimental Evidence Suggesting That Glucocorticoids Contrimentioning

confidence: 99%

Interaction Between the Hypothalamic—Pituitary—Adrenal Axis and Behavioural Compensation Following Unilateral Vestibular Deafferentation

Gliddon

Smith

Darlington

2003

Vestibular compensation is defined as the process of behavioural recovery that occurs following the loss of sensory input from one or both vestibular labyrinths. The visual and postural instability resulting from the vestibular damage must alter the homeostasis of the subject; however, very little research has been conducted that investigates the interaction between vestibular compensation and the adaptive stress response of the body, i.e. the hypothalamic-pituitary-adrenal (HPA) axis. The aim of this review is to describe and evaluate the experimental evidence indicating a link between vestibular compensation and the body's response to stress, via the HPA axis.