title: Cytosolic glucocorticoid receptor expression in the rat vestibular nucleus and hippocampus following unilateral vestibular deafferentation.
abstract: It has been suggested that vestibular compensation, the process of behavioural recovery that occurs following peripheral vestibular damage, might be partially dependent on the release of glucocorticoids (GC) during the early stages of recovery from the lesion. One possibility is that glucocorticoid receptors (GRs) in the vestibular nucleus complex (VNC) might change following the lesion, altering their response to GCs. We sought to test this hypothesis by quantifying the expression of cytosolic GRs in the bilateral VNCs at 10 h, 58 h and 2 weeks following unilateral vestibular deafferentation (UVD) in rat, using western blotting. We also examined GR expression in the CA1, CA2/3 and dentate gyrus (DG) subregions of the hippocampus and measured serum corticosterone levels. Compared with sham surgery and anaesthetic controls, we found no significant changes in GR expression in the ipsilateral or contralateral VNCs at any time post-UVD. However, we did find a significant decrease in GR expression in the ipsilateral CA1 at 2 weeks post-UVD. Serum corticosterone levels were significantly lower in all groups at 58 h post-op. compared to 10 h and 2 weeks; however, there were no significant differences between the UVD and control groups at any time point. These results suggest that changes in GR expression in the VNC are unlikely to contribute to the development of vestibular compensation. However, long-term changes in GR expression in CA1 might be related to chronic deficits in hippocampal function and spatial cognition following vestibular damage.
authors.affiliation: Department of Pharmacology and Toxicology, School of Medical Sciences, University of Otago Medical School, Dunedin, Dunedin, New Zealand.
authors.forename: Libby
authors.initials: L
authors.lastname: Lindsay
authors.forename: Ping
authors.initials: P
authors.lastname: Liu
authors.forename: Catherine
authors.initials: C
authors.lastname: Gliddon
authors.forename: Yiwen
authors.initials: Y
authors.lastname: Zheng
authors.forename: Paul F
authors.initials: PF
authors.lastname: Smith
authors.forename: Cynthia L
authors.initials: CL
authors.lastname: Darlington
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology*; D000344:Afferent Pathways / Q000378:metabolism / Q000503:physiopathology; D000818:Animals; D003348:Cortisone / Q000097:blood; D003600:Cytosol / Q000378:metabolism; D003714:Denervation; D007839:Functional Laterality / Q000502:physiology; D006624:Hippocampus / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D008569:Memory Disorders / Q000209:etiology / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D011965:Receptors, Glucocorticoid / Q000378:metabolism*; D020127:Recovery of Function / Q000502:physiology*; D015837:Vestibular Diseases / Q000150:complications / Q000503:physiopathology; D014726:Vestibular Nuclei / Q000378:metabolism* / Q000503:physiopathology; D014722:Vestibule, Labyrinth / Q000294:innervation / Q000502:physiology* / Q000601:surgery
chemical_list: D011965:Receptors, Glucocorticoid; D003348:Cortisone