Changes in nitric oxide synthase-like immunoreactivities in unipolar brush cells in the rat cerebellar flocculus after unilateral labyrinthectomy.

To elucidate the role of nitric oxide (NO)-mediated signaling in vestibular compensation, we examined effects of unilateral labyrinthectomy (UL) on the neuronal isoform of NO synthase (NOS) expression in the rat central vestibular system using immunohistochemical techniques. After UL, a substantial number of NOS-like immunoreactive (-LIR) neurons were observed in the granule cell layer in bilateral flocculi, and these neurons were determined to be unipolar brush cells (UB cells) by their unique morphology and location. NOS-LIR UB cells appeared by 12 h with a maximum increase in number 24 h after UL, and then gradually disappeared in accordance with the development of vestibular compensation. Continuous floccular infusion of N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOS, or 2-phenyl-4,4,5,5-tetramethyl-1-oxyl-3-oxide (PTIO), an inhibitor of NO, caused more severe vestibulo-ocular deficits at the initial stage after UL and slightly delayed the recovery from these symptoms. All these findings suggest that up-regulation of NO production in floccular UB cells facilitates vestibular compensation, especially at the initial stage after UL.