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The Journal of Neuroscience, 0000, 20:RC96:1-5
RAPID COMMUNICATION
Memory Consolidation of Auditory Pavlovian Fear Conditioning
Requires Protein Synthesis and Protein Kinase A in the
Amygdala
Glenn E.
Schafe and
Joseph E.
LeDoux
W. M. Keck Foundation Laboratory of Neurobiology, Center for
Neural Science, New York University, New York, New York, 10003
Previous studies have shown that long-term potentiation (LTP) can
be induced in the lateral nucleus of the amygdala (LA) after stimulation of central auditory pathways and that auditory fear conditioning modifies neural activity in the LA in a manner similar to
LTP. The present experiments examined whether intra-LA administration of inhibitors of protein synthesis or protein kinase A (PKA)
activity, treatments that block LTP in hippocampus, interfere with
memory consolidation of fear conditioning. In the first series of
experiments, rats received a single conditioning trial followed
immediately by intra-LA infusions of anisomycin (a protein synthesis
inhibitor) or Rp-cAMPS (an inhibitor of PKA activity) and were tested
24 hr later. Results indicated that immediate post-training infusion of
either drug dose-dependently impaired fear memory retention, whereas
infusions 6 hr after conditioning had no effect. Additional experiments
showed that anisomycin and Rp-cAMPS interfered with long-term memory
(LTM), but not short-term memory (STM), of fear and that the effect on
LTM was specific to memory consolidation processes rather than to
deficits in sensory or performance processes. Findings suggest that the
LA is essential for memory consolidation of auditory fear conditioning
and that this process is PKA and protein-synthesis dependent.
Key words:
fear; amygdala; LTP; memory consolidation; cAMP; protein
synthesis
Copyright © 0000 Society for Neuroscience 0270-6474/00/$05.00/0
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