| Project/Area Number |
16300133
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurophysiology and muscle physiology
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| Research Institution | Tottori University |
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Principal Investigator |
HATA Yoshio Tottori Univ., Grad.Sch.Med.Sci., Professor, 大学院医学系研究科, 教授 (40212146)
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| Co-Investigator(Kenkyū-buntansha) |
ICHISAKA Satoshi Tottori Univ., Fac.Med., Research Associate, 医学部, 助手 (50359874)
SATO Takemasa Tottori Univ., Fac.Med., Research Associate, 医学部, 助手 (80346345)
AKASAKI Takafumi Tottori Univ., Grad.Sch.Med.Sci., Research Associate, 大学院医学系研究科, 助手 (30335393)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥12,800,000 (Direct Cost: ¥12,800,000)
Fiscal Year 2006: ¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 2005: ¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥6,700,000 (Direct Cost: ¥6,700,000)
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| Keywords | Ocular dominance / Plasticity / Postnatal development / Monocular deprivation / Visual cortex / Critical period / Hebb rule / 抑制 / 一次視覚野 |
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| Research Abstract |
Monocular visual deprivation (MD) in the early postnatal life causes a significant loss of cortical responses to a deprived eye and a retraction of geniculocortical axons serving the deprived eye (ocular dominance plasticity). On the other hand, when MD is combined with a pharmacological inhibition of the visual cortex by administering a GABAA agonist, muscimol, cortical neurons lose their responses to an open eye. Furthermore, active arbors serving an open eye selectively retract, whereas the branches of arbors from a deprived eye remain mostly intact, suggesting that uncorrelated activity between presynaptic inputs and cortical neurons leads to the pruning of afferent axons. To clarify the mechanism of ocular dominance plasticity in the inhibited cortex. we tested whether it has characteristics, such as age-dependency, similar to the plasticity in the normal cortex.
Muscimol-treatment of adult visual cortex did not induce a loss of open eye response, suggesting that the ocular dominan
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ce plasticity in the inhibited cortex operates only in developing animals as in the normal cortex. Further study showed that the ocular dominance plasticity proceeds in slower time course than in the normal cortex. Three days MD did not induce the ocular dominance plasticity in the inhibited cortex, while it exerted a saturated effect in the normal cortex.
Binocular deprivation (BD) exerts a much weaker effect on cortical responses than MD and does not induce the retraction of afferent axons. Thus, we examined whether the retraction of geniculocortical axons in an inhibited cortex could be induced in the absence of binocular imbalance. We analyzed the morphology of geniculocortical axons in a pharmacologically inhibited visual cortex of animals with normal vision and binocularly deprived animals. In the normal vision animals, the axonal arbors in the inhibited cortex showed robust retraction. On the other hand, the arbors in binocularly deprived animals remained mostly intact. These results suggest that a homosynaptic associative mechanism, rather than a heterosynaptic competition between inputs, may play an important role in the ocular dominance plasticity. Less
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