Synaptic Modulation via Basolateral Amygdala on the Rat Hippocampus–Medial Prefrontal Cortex Pathway in Fear Extinction
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- Inoue Sumitaka
- Department of Pharmacology, School of Pharmaceutical Science, Health Sciences University of Hokkaido, Japan
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- Kamiyama Hidekazu
- Department of Pharmacology, School of Pharmaceutical Science, Health Sciences University of Hokkaido, Japan
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- Matsumoto Machiko
- Department of Pharmacology, School of Pharmaceutical Science, Health Sciences University of Hokkaido, Japan
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- Yanagawa Yoshiki
- Department of Pharmacology, School of Pharmaceutical Science, Health Sciences University of Hokkaido, Japan
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- Hiraide Sachiko
- Department of Pharmacology, School of Pharmaceutical Science, Health Sciences University of Hokkaido, Japan
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- Saito Yasuhiro
- Department of Pharmacology, School of Pharmaceutical Science, Health Sciences University of Hokkaido, Japan
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- Shimamura Kei-ichi
- Department of Pharmacology, School of Pharmaceutical Science, Health Sciences University of Hokkaido, Japan
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- Togashi Hiroko
- Department of Pharmacology, School of Pharmaceutical Science, Health Sciences University of Hokkaido, Japan
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The present study elucidated the functional role of modulatory effects of basolateral amygdala (BLA) on synaptic transmission in the rat hippocampus–medial prefrontal cortex (mPFC) pathway, compared with the hippocampal dentate gyrus (DG). Exposure to conditioned fear stress (CFS) or prior BLA activation enhanced tetanus-induced long-term potentiation (LTP) in DG. A similar synaptic response was found by low frequency stimulation (LFS) prior to tetanus. In mPFC, they did not affect LTP, but prior BLA activation, as well as pretreatment with the N-methyl-d-aspartate (NMDA)-receptor antagonist MK-801 (0.1 mg/kg, i.p.), suppressed LFS-primed LTP. This BLA-mediated synaptic pattern was mimicked by synaptic changes observed in the fear extinction process; prior BLA activation suppressed the synaptic potentiation responsible for extinction retrieval and attenuated decreases in fear-related freezing behavior. These data suggest that LFS-primed LTP in mPFC is related to the neural basis of extinction. Extinction-related synaptic potentiation did not occur in a juvenile stress model that exhibited extinction deficit. In addition, LFS-primed LTP was suppressed in this model, which was reversed by the NMDA-receptor agonist d-cycloserine (15 mg/kg, i.p.). These findings suggest that modulatory effects of BLA on synaptic function in the hippocampus–mPFC pathway play a significant role in fear extinction in rats.
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 123 (3), 267-278, 2013
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390282680158171904
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- NII論文ID
- 130003382607
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- NII書誌ID
- AA11806667
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- COI
- 1:STN:280:DC%2BC2c7islartQ%3D%3D
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 025038248
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- PubMed
- 24189655
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
- KAKEN
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- 抄録ライセンスフラグ
- 使用不可