Author:
Rastoldo Guillaume,Marouane Emna,El Mahmoudi Nada,Pericat David,Watabe Isabelle,Lapotre Agnes,Tonetto Alain,López-Juárez Alejandra,Caron Philippe,Fraysse Marie-José Esteve,Zwergal Andreas,Tighilet Brahim
Abstract
AbstractUnilateral vestibular lesions induce a vestibular syndrome, which recovers over time due to vestibular compensation. The therapeutic effect of L-Thyroxine (L-T4) on vestibular compensation was investigated by behavioral testing and immunohistochemical analysis in a rat model of unilateral vestibular neurectomy (UVN). We demonstrated that an acute L-T4 treatment reduced the vestibular syndrome and significantly promoted vestibular compensation. Thyroid hormone receptors (TRα and TRβ) and type II iodothyronine deiodinase (DIO2) were present in the vestibular nuclei (VN), supporting a local action of L-T4. We confirmed the T4-induced metabolic effects by demonstrating an increase in the number of cytochrome oxidase-labelled neurons in the VN three days after the lesion. L-T4 treatment modulated glial reaction by decreasing both microglia and oligodendrocytes in the deafferented VN three days after UVN and increased cell proliferation. The survival of newly generated cells was not affected, but neuronal differentiation was altered by the L-T4 treatment.
Publisher
Cold Spring Harbor Laboratory
Cited by
1 articles.
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