Spatio-temporal changes on c-Fos protein expression were investigated in vestibular compensation following unilateral labyrinthectomy (UL) induced by injection of arsanilate into the middle ear cavity, chemical labyrinthectomy, or surgical labyrinthectomy in medial vestibular nuclei (MVN), prepositus hypoglossal nuclei (PrH), and inferior olivary nuclei (ION) of Sprague-Dawley rats. Number of spontaneous nystagmus in surgical labyrinthectomy group was 28.2+/-.2 beats/10 sec at post-op 2 hs and the nystagmus disappeared 76 hs after UL. In chemical labyrinthectomy group, spontaneous nystagmus occurred 6 hs after UL and increased up to maximum at 12 hs and disappeared 96 hs. Head deviation in surgical labyrinthectomy group reached a peak at post-op 2 hs and recovered to control level at 144 hs, but chemical labyrinthectomy produced head deviation 24 hs after UL and increased degree of the deviation over time till 144 hs. Expression of c-Fos protein in surgical labyrinthectomy group at post-op 2 hs was 81+/-9.4 cells in ipsilateral MVN to the lesion side and 212+/-0 cells in contralateral MVN, which showed severe asymmetry between bilateral MVN, and decrease of c-Fos protein expression was more in contralateral MVN than in ipsilateral MVN at 6 hs. Chemical labyrinthectomy expressed more c-Fos protein in contralateral MVN 6 hs after UL and in ipsilateral MVN 12 hs after UL, which showed asymmetry of c-Fos protein expression between bilateral MVN. And the expression in ipsilateral MVN of chemical labyrinthectomy group was increased gradually 48 hs after UL and reached a peak at 72 hs. In chemical labyrinthectomy group, expression of c-Fos protein in PrH was increased more in ipsilateral than in contralateral 6 hs after UL and more in contralateral 12 hs after UL, and ION showed more expression of c-Fos protein in contralateral than in ipsilateral 6 hs after UL through 72 hs. These results suggest that the course of vestibular compensation and the temporal expression of c-Fos protein in the brain stem nuclei following UL differed between surgical and chemical labyrinthectomy.
Animals ; Arsanilic Acid ; Brain Stem* ; Brain* ; Compensation and Redress ; Ear, Middle ; Head ; Rats* ; Rats, Sprague-Dawley ; Vestibular Nuclei

This study was performed to assess the neurotoxic effects of methylmercury, arsanilic acid and danofloxacin by quantification of neural-specific proteins in vitro. Quantitation of the protein markers during 14 days of differentiation indicated that the mouse ESCs were completely differentiated into neural cells by Day 8. The cells were treated with non-cytotoxic concentrations of three chemicals during differentiation. Low levels of exposure to methylmercury decreased the expression of GABAA-R and Nestin during the differentiating stage, and Nestin during the differentiated stage. In contrast, GFAP, Tuj1, and MAP2 expression was affected only by relatively high doses during both stages. Arsanilic acid affected the levels of GABA(A)-R and GFAP during the differentiated stage while the changes of Nestin and Tuj1 were greater during the differentiating stage. For the neural markers (except Nestin) expressed during both stages, danofloxacin affected protein levels at lower concentrations in the differentiated stage than the differentiating stage. Acetylcholinesterase activity was inhibited by relatively low concentrations of methylmercury and arsanilic acid during the differentiating stage while this activity was inhibited only by more than 40 microM of danofloxacin in the differentiated stage. Our results provide useful information about the different toxicities of chemicals and the impact on neural development.
Acetylcholinesterase/metabolism ; Animals ; Arsanilic Acid/*toxicity ; Cell Differentiation/*drug effects ; Embryonic Stem Cells/cytology/*drug effects ; Environmental Pollutants/*toxicity ; Fluorescent Antibody Technique ; Fluoroquinolones/*toxicity ; Gene Expression Regulation/drug effects ; Methylmercury Compounds/*toxicity ; Mice ; Nerve Tissue Proteins/metabolism ; Neurons/cytology/*drug effects ; Tetrazolium Salts/metabolism ; Thiazoles/metabolism