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.
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Acknowledgements
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).
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Supplementary information
Supplementary Fig. 1
Behavioral Paradigms. Schematic outline of the behavioral paradigms used in Experiment #1 (in situ hybridization experiment), (A), Experiment #2 (B), and Experiment #3 (C). (PDF 44 kb)
Supplementary Fig. 2
The CB1 antagonist rimonabant impairs within-session extinction. (PDF 90 kb)
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Chhatwal, J., Stanek-Rattiner, L., Davis, M. et al. Amygdala BDNF signaling is required for consolidation but not encoding of extinction. Nat Neurosci 9, 870–872 (2006). https://doi.org/10.1038/nn1718
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DOI: https://doi.org/10.1038/nn1718
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