Roles of amygdala glucocorticoid receptor in stress-modulated fear conditioning
Project/Area Number |
15K06705
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Neurophysiology / General neuroscience
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Research Institution | University of Toyama |
Principal Investigator |
Inoue Ran 富山大学, 大学院医学薬学研究部(医学), 助教 (70401817)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
Keywords | 扁桃体 / グルココルチコイド受容体 / 恐怖記憶 / メタ可塑性 / cue依存的恐怖記憶 / ストレス / 扁桃体外側核 |
Outline of Final Research Achievements |
The lateral nucleus of the amygdala (LA) is a key structure underlying auditory-cued fear conditioning. Glucocorticoid receptor (GR) is crucial for signaling mediated by stress-induced high levels of glucocorticoids. Here, we demonstrate that genetic disruption of GR in the LA (LAGRKO) resulted in an auditory-cued fear memory deficit for strengthened conditioning. Furthermore, the suppressive effect of a single restraint stress (RS) prior to conditioning on auditory-cued fear memory in floxed GR (control) mice was abolished in LAGRKO mice. Optogenetic induction of long-term depression (LTD) at LA reduced fear memory in RS-exposed LAGRKO mice, and in contrast, induction of long-term potentiation (LTP) increased fear memory in RS-exposed floxed GR mice. These findings suggest that prior stress suppresses fear conditioning-induced LTP at auditory inputs to the LA in a GR-dependent manner, thereby protecting animals from encoding excessive cued fear memory under stress conditions.
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Report
(4 results)
Research Products
(5 results)