Cytosolic glucocorticoid receptor expression in the rat vestibular nucleus and hippocampus following unilateral vestibular deafferentation.
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.
Lindsay
Libby
L
Department of Pharmacology and Toxicology, School of Medical Sciences, University of Otago Medical School, Dunedin, Dunedin, New Zealand.
Liu
Ping
P
Gliddon
Catherine
C
Zheng
Yiwen
Y
Smith
Paul F
PF
Darlington
Cynthia L
CL
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
D011965:Receptors, Glucocorticoid; D003348:Cortisone