2013 Fiscal Year Final Research Report
Morphological analysis of the GABA function using knockout mice lacking of molecules involved in GABAergic signaling
| Project/Area Number |
23500413
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | University of the Ryukyus |
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Principal Investigator |
TAKAYAMA Chitoshi 琉球大学, 医学(系)研究科(研究院), 教授 (60197217)
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| Co-Investigator(Renkei-kenkyūsha) |
YANAGAWA Yuchio 群馬大学, 大学院・医学研究科, 教授 (90202366)
OKABE Akihito 琉球大学, 大学院・医学研究科, 准教授 (10313941)
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| Project Period (FY) |
2011 – 2013
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| Keywords | GABAergic signaling / GAD / VGAT / KCC2 / GABAergic synapse / GABA transporter / spinal cord / calbindin |
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| Research Abstract |
1.We investigated the ontogeny of GABAergic neurons, GABAergic synapses, and GABA removal system in the developing mouse spinal cord as the normal control of knockout mice.2.We investigated the changes in GABAergic signaling during degeneration and regeneration of hypoglossal and facial nerves. We found that GABAergic signaling changed to the immatute form during regeneration, suggesting that GABA may act as an excitatory transmitter and be involved in regeneration of axons.3.We morphologically investigated the knockout mice lacking three molecules involved in GABAergic signaling, glutamic acid decarboxylase (GAD), vesicular GABA transporter (VGAT), and potassium chloride cotransporter (KCC2). We found that the number and localization of calbindin-positive or calretinin-positive interneurons in the dorsal horn of spinal cord of three types of knockout mice, suggesting that GABA might be involved in migration and proliferation of interneurons in the spinal cord during development.
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Research Products
(29 results)
