Plasticity of cortical neurons in the developing visual cortex.
| Project/Area Number |
14580789
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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 |
神経・脳内生理学
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| Research Institution | Tottori University Graduate School |
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Principal Investigator |
HATA Yoshio Tottori University Graduate School of Medical Sciences, Professor, 大学院・医学系研究科, 教授 (40212146)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥4,200,000 (Direct Cost: ¥4,200,000)
Fiscal Year 2003: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2002: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | VISUAL CORTEX / OCULAR DOMINANCE / VISUAL DEPRIVATION / DEVELOPMENT / PLASTICITY / CAT |
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| Research Abstract |
Neural circuits in the mammalian neocortex are modified by experience-induced neural activity during postnatal development. Monocular deprivation (MD) during early postnatal life remodels neural circuits of the primary visual cortex so that most neurons respond poorly to stimuli presented to the deprived eye and thalamic input from this eye is ultimately retracted. Although this remodeling has been thought to be initiated at thalamocortical synapses in cortical layer IV, recent experiments showed that physiological plasticity proceeds earlier in supragranular layers than in layer IV of the cortex. These findings suggest a possibility that thalamocortical reorganization is guided by earlier changes in intracortical connections. However, it is still unknown what type of modification in the cortical circuit underlies this rapid plasticity in supragranular layers. To address this question, the present research aimed to explore morphological plasticity of the intracortical ascending axons from layer IV to III, which give strong excitatory inputs to supragranular cells. Also we examined cortical content of neurotrophins which play a role in neurite extension. Optical imaging of the intrinsic signal allowed us to identify the ocular dominance columns and to inject a retrograde tracer inlayer III at the border of the ocular dominance columns. By injecting two retrograde tracers at the same location before and after MD, we examined a possible change in the distribution of labeled layer IV cells in relation to the ocular dominance column pattern. The number of labeled cells decreased in the deprived eye columns after MD in some cases. MD also decreased protein level of brain-derived neurotrophic factor in the visual cortex. These results show a possibility that MD might induce a retraction of intracortical axons serving the deprived eye and that BDNF might contribute to the retraction.
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Report
(3 results)
Research Products
(20 results)
