Project/Area Number |
26430022
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Neurophysiology / General neuroscience
|
Research Institution | Saitama Medical University |
Principal Investigator |
Chiaki Itami 埼玉医科大学, 医学部, 講師 (90392430)
|
Co-Investigator(Kenkyū-buntansha) |
木村 文隆 大阪大学, 医学系研究科, 准教授 (00202044)
|
Research Collaborator |
LU Hui-chen インディアナ大学, 教授
HUANG J-Y インディアナ大学, 研究員
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
Keywords | 体性感覚野 / スパイクタイミング可塑性8(STDP) / カンナビノイド / スパイクタイミング可塑性 / CB1受容体 / バレル皮質 / STDP / LTD / 臨界期 / スパイクタイミング依存性可塑性 / カンナビノイド受容体 / 活動依存性 / シナプス刈り込み |
Outline of Final Research Achievements |
Activation of cannabinoid CB1 receptors (CB1Rs) causes both physiological and morphological effects on the development of neuronal circuits. In the rodent barrel cortex, CB1R is required for the long-term depression (LTD) component of spike timing-dependent plasticity (STDP). We showed that CB1R activation caused LTD in a spike timing-dependent manner (t-LTD) at thalamocortical terminals. Since CB1R knockout (KO) mice showed disrupted thalamocortical projection, we concluded that endogenous CB1R signalling is important in translating physiological changes into morphological consequences.
|