Delayed Noradrenergic Activation in the Dorsal Hippocampus Promotes the   Long-Term Persistence of Extinguished Fear

doi:10.1038/npp.2014.42

CORC > 北京大学 > 生命科学学院

	Delayed Noradrenergic Activation in the Dorsal Hippocampus Promotes the Long-Term Persistence of Extinguished Fear
	Chai, Ning ; Liu, Jian-Feng ; Xue, Yan-Xue ; Yang, Chang ; Yan, Wei ; Wang, Hui-Min ; Luo, Yi-Xiao ; Shi, Hai-Shui ; Wang, Ji-Shi ; Bao, Yan-Ping ; Meng, Shi-Qiu ; Ding, Zeng-Bo ; Wang, Xue-Yi ; Lu, Lin
刊名	neuropsychopharmacology
	2014
关键词	REQUIRES PROTEIN-SYNTHESIS KINASE ANCHORING PROTEINS NUCLEUS-ACCUMBENS CORE CONDITIONED FEAR MEMORY CONSOLIDATION BASOLATERAL AMYGDALA CONTEXTUAL FEAR SIGNALING PATHWAY PREFRONTAL CORTEX D-CYCLOSERINE
DOI	10.1038/npp.2014.42
英文摘要	Fear extinction has been extensively studied, but little is known about the molecular processes that underlie the persistence of extinction long-term memory (LTM). We found that microinfusion of norepinephrine (NE) into the CAI area of the dorsal hippocampus during the early phase (0 h) after extinction enhanced extinction LTM at 2 and 14 days after extinction. lntra-CA I infusion of NE during the late phase (12 h) after extinction selectively promoted extinction LTM at 14 days after extinction that was blocked by the beta-receptor antagonist propranolol, protein kinase A (PKA) inhibitor Rp-cAMPS, and protein synthesis inhibitors anisomycin and emetine. The phosphorylation levels of PKA, cyclic adenosine monophosphate response element-binding protein (CREB), GluR I, and the membrane GluRI level were increased by NE during the late phase after extinction that was also blocked by propranolol and Rp-cAMPS. These results suggest that the enhancement of extinction LTM persistence induced by NE requires the activation of the)beta-receptor/PKA/CREB signaling pathway and membrane GluR I trafficking. Moreover, extinction increased the phosphorylation levels of Erk1/2, CREB, and GluR I, and the membrane GluR I level during the late phase, and anisomycin/emetine alone disrupted the persistence of extinction LTM, indicating that the persistence of extinction LTM requires late-phase protein synthesis in the CA I. Propranolol and Rp-cAMPS did not completely disrupt the persistence of extinction LTM, suggesting that another)beta-receptor/PKA-independent mechanism underlies the persistence of extinction LTM. Altogether, our results showed that enhancing hippocampal noradrenergic activity during the late phase after extinction selectively promotes the persistence of extinction LTM.; http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000337550600015&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701 ; Neurosciences; Pharmacology & Pharmacy; Psychiatry; SCI(E); PubMed; 7; ARTICLE; ydyywxy@163.com; linlu@bjmu.edu.cn; 8; 1933-1945; 39
语种	英语
内容类型	期刊论文
源URL	[http://ir.pku.edu.cn/handle/20.500.11897/189452]
专题	生命科学学院心理与认知科学学院
推荐引用方式 GB/T 7714	Chai, Ning,Liu, Jian-Feng,Xue, Yan-Xue,et al. Delayed Noradrenergic Activation in the Dorsal Hippocampus Promotes the Long-Term Persistence of Extinguished Fear[J]. neuropsychopharmacology,2014.
APA	Chai, Ning.,Liu, Jian-Feng.,Xue, Yan-Xue.,Yang, Chang.,Yan, Wei.,...&Lu, Lin.(2014).Delayed Noradrenergic Activation in the Dorsal Hippocampus Promotes the Long-Term Persistence of Extinguished Fear.neuropsychopharmacology.
MLA	Chai, Ning,et al."Delayed Noradrenergic Activation in the Dorsal Hippocampus Promotes the Long-Term Persistence of Extinguished Fear".neuropsychopharmacology (2014).