2004 Fiscal Year Final Research Report Summary
Morphological and functional investigation of vestibular compensation
| Project/Area Number |
15591808
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
TSUJI Jun KYOTO UNIVERSITY, Graduate School of medicine, Lecturer, 医学研究科, 講師 (30252448)
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| Co-Investigator(Kenkyū-buntansha) |
ITO Juichi KYOTO UNIVERSITY, Graduate School of medicine, Professor, 医学研究科, 教授 (90176339)
NAKAGAWA Takayuki KYOTO UNIVERSITY, Graduate School of medicine, Assistant Professor, 医学研究科, 助手 (50335270)
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| Project Period (FY) |
2003 – 2004
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| Keywords | plasticity / vestibular compensation / mouse / immunohistology / c-Fos / visual suppression |
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| Research Abstract |
Vestibular compensation is attributed to functional and structural reorganization of neural networks in the central vestibular system, but its precise mechanism is still not clear. Immediate early gene c-Fos is used as a marker of neuronal activation, because of its very limited expression in the normal state and quick appearance after stimulation. Previous reports, investigating c-Fos expression after unilateral labyrinthectomy were made in rats and guinea pigs, but not in the mouse brainstem. For future application to the gene knockout mouse, we examined c-Fos expression in the mouse after unilateral labyrinthectomy. Twenty-four hours after surgery, a highest number of c-Fos positive cells were observed in the bilateral medial vestibular nucleus (Mve), spinal vestibular nucleus (SpVe) and in the contra lateral prepositus hypoglossal nucleus (PrH). In the inferior olive nucleus (IO), c-Fos positive cells were significantly higher in the intact side. Our results suggest that PrH nuclea
… More
r cells are activated., and the neural integrator might be modified. in vestibular compensation period, thus adjust the VOR gains.
It is well known that the fixating mechanism of visual system influences nystagmus of vestibular origin. Nystagmus induced by caloric stimulation in dark is reduced in light (visual suppression). And it is generally assumed that floccular Purkinje cells encodes retinal slip and controls the gain of the horizontal vestibulo-ocular reflex. Previous reports showed that lesions in the flocculus abolish visual suppression. However the precise mechanism of the visual suppression is not completely understood. In the present study, we recorded the visual suppressions in mutant mice deficient in the delta 2 subunit of the ionotrphhic glutamate receptor (GluR delta-2) in Purkinje cells to investigate the role of glutaminergic system on the control of VOR. Wild type and homozygous mutant mice GluR delta-2(-/-) 6-10 week old were used. The left eye was illuminated by an infrared LED and monitored by an infrared CCD camera. Eye movements were captured and analyzed by a computer. The pupil was fitted as an ellipse and the horizontal eye angular movement was calculated using the shape and direction of ellipse (Iwashita et al. 2001). Caloric stimulation was made by injection of 5-ml ice cold water into the left external ear canal in dark and light. In wild type the slow phase velocity in dark was reduced about 90 % in light. In GluR delta-2(-/-) mice the velocity was reduced very little (10 %), no change or even increased in light. These results suggest that the parallel fiber input to floccular Purkinje cells mediated by ionotrophic glutamate receptor play important roles in the visual suppression of the vestibular nystagmus. Less
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