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.
Publication types
-
Comparative Study
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
-
Amygdala / metabolism*
-
Animals
-
Behavior, Animal
-
Brain-Derived Neurotrophic Factor / genetics
-
Brain-Derived Neurotrophic Factor / metabolism*
-
Cannabinoid Receptor Antagonists
-
Conditioning, Classical / drug effects
-
Conditioning, Classical / physiology*
-
Extinction, Psychological / physiology
-
Gene Expression / drug effects
-
Gene Expression / physiology
-
Genetic Vectors / physiology
-
Green Fluorescent Proteins / biosynthesis
-
Immunohistochemistry / methods
-
Lentivirus / physiology
-
Male
-
Piperidines / pharmacology
-
Pyrazoles / pharmacology
-
RNA, Messenger / metabolism
-
Rats
-
Rats, Sprague-Dawley
-
Receptor, trkB / physiology
-
Reflex, Startle / drug effects
-
Reflex, Startle / physiology
-
Rimonabant
-
Signal Transduction / drug effects
-
Signal Transduction / physiology*
-
Time Factors
Substances
-
Brain-Derived Neurotrophic Factor
-
Cannabinoid Receptor Antagonists
-
Piperidines
-
Pyrazoles
-
RNA, Messenger
-
Green Fluorescent Proteins
-
Receptor, trkB
-
Rimonabant