4.7 Article

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

Journal

NATURE NEUROSCIENCE
Volume 9, Issue 7, Pages 870-872

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/nn1718

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Funding

  1. NCRR NIH HHS [P51 RR000165-460189, P51RR000165, P51 RR000165-457288, P51 RR000165, P51 RR000165-450216] Funding Source: Medline
  2. NIDA NIH HHS [R01 DA019624-01A2, R01 DA019624] Funding Source: Medline
  3. NIGMS NIH HHS [T32 GM008169] Funding Source: Medline
  4. NIMH NIH HHS [R01 MH047840, K01 MH069884-02, F30 MH070218, MH070218, K01 MH069884, K01 MH069884-03, K01 MH069884-01, R37 MH047840, MH47840, MH069884] Funding Source: Medline

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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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