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杏仁核脑源性神经营养因子信号传导是记忆巩固所必需的，但不是消退记忆编码所必需的。

Amygdala BDNF signaling is required for consolidation but not encoding of extinction.

作者信息

Chhatwal Jasmeer P, Stanek-Rattiner Lisa, Davis Michael, Ressler Kerry J

机构信息

Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, 1639 Pierce Drive, Suite 4000, Atlanta, Georgia 30322, USA.

出版信息

Nat Neurosci. 2006 Jul;9(7):870-2. doi: 10.1038/nn1718. Epub 2006 Jun 18.

DOI:10.1038/nn1718
PMID:16783370
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2562628/
Abstract

Brain-derived neurotrophic factor (BDNF) acting through the tyrosine kinase B receptor (TrkB) is thought to be a critical mediator of learning. As there are no available selective antagonists of TrkB, we used a lentivirus encoding a dominant-negative TrkB (TrkB.t1) to antagonize BDNF signaling during extinction of conditioned fear. Whereas TrkB.t1-infected rats showed normal within-session extinction, their retention of extinction was impaired, suggesting that amygdala TrkB activation is required for the consolidation of stable extinction memories.

摘要

脑源性神经营养因子（BDNF）通过酪氨酸激酶B受体（TrkB）发挥作用，被认为是学习的关键调节因子。由于目前尚无可用的TrkB选择性拮抗剂，我们使用了一种编码显性负性TrkB（TrkB.t1）的慢病毒，在条件性恐惧消退过程中拮抗BDNF信号传导。虽然感染TrkB.t1的大鼠在训练过程中的消退表现正常，但其消退记忆的保持受损，这表明杏仁核TrkB激活是稳定消退记忆巩固所必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/412a/2562628/8431f340cb11/nihms-55890-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/412a/2562628/993409918675/nihms-55890-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/412a/2562628/8431f340cb11/nihms-55890-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/412a/2562628/993409918675/nihms-55890-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/412a/2562628/8431f340cb11/nihms-55890-f0002.jpg

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