| Project/Area Number |
21591530
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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 |
Psychiatric science
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| Research Institution | Health Sciences University of Hokkaido |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TOGASHI Hiroko 北海道医療大学, 薬学部, 教授 (20113590)
木村 真一 北海道医療大学, 薬学部, 講師 (90281287)
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| Co-Investigator(Renkei-kenkyūsha) |
KIMURA Shin-ichi 北海道医療大学, 薬学部, 講師 (90281287)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 脳機能発達 / 幼児期ストレス / 神経可塑性 / 臨界期 / ERK活性 / 恐怖記憶 / セロトニン / メタ可塑性 / 幼若期ストレス / 心的外傷後ストレス |
|---|
| Research Abstract |
The present study demonstrated that early postnatal stress caused extinction deficit in adult rats, in which "critical period" exists during brain development. This extinction deficit appears to be associated with dysfunction of hippocampal CA1 field and/or medial prefrontal cortex(mPFC), because synaptic potentiation and ERK activation induced by extinction processes, in a brain specific manner, did not occur in juvenile stress model rats. This impaired synaptic plasticity and suppressed ERK activity, in addition to behavioral deficit were ameliorated by pretreatment with a NMDA receptor agonist D-cycloserine. These results suggest that the different phenotypes in adulthood result from neurodevelopmental perturbations of neural circuits of emotional regulation that elicited by early life stress.
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