Memory consolidation of auditory Pavlovian fear conditioning requires protein synthesis and protein kinase A in the amygdala

Previous studies have shown that long-term potentiation (LTP) can be induce d in the lateral nucleus of the amygdala (LA) after stimulation of central auditory pathways and that auditory fear conditioning modifies neural activ ity in the LA in a manner similar to LTP. The present experiments examined whether intra-LA administration of inhibitors of protein synthesis or prote in kinase A (PKA) activity, treatments that block LTP in hippocampus, inter fere with memory consolidation of fear conditioning. In the first series of experiments, rats received a single conditioning trial followed immediatel y 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-depende ntly impaired fear memory retention, whereas infusions 6 hr after condition ing had no effect. Additional experiments showed that anisomycin and Rp-cAM PS 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 pr ocesses rather than to deficits in sensory or performance processes. Findin gs suggest that the LA is essential for memory consolidation of auditory fe ar conditioning and that this process is PKA and protein-synthesis dependen t.