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

• Type of Material: Article
• Authors: Jasmeer P Chhatwal, Emory University; Lisa Stanek-Rattiner, Emory University; Michael Davis, Emory University; Kerry J Ressler, Emory University
• Language: English
• Date: 2006-07
• Publisher: Nature Research (part of Springer Nature)
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2006, Rights Managed by Nature Publishing Group
• Final Published Version (URL): http://www.nature.com/neuro/journal/v9/n7/full/nn1718.html
• Title of Journal or Parent Work: Nature Neuroscience
• ISSN: 1097-6256
• Volume: 9
• Issue: 7
• Start Page: 870
• End Page: 872
• Grant/Funding Information: The authors declare no competing financial interests.; Support was provided by the US National Institutes of Health (MH47840 to M.D., MH069884 to K.J.R. and MH070218 to J.P.C.), the National Alliance for Research on Schizophrenia and Depression (NARSAD; K.J.R.), NIH/NCRR base grant (P51RR000165) to Yerkes National Primates Research Center and the Center for Behavioral Neuroscience (National Science Foundation agreement IBN-987675).
• Research Categories: Psychology, Behavioral; Biology, Neuroscience

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.