Publication | Open Access
Memory Consolidation of Auditory Pavlovian Fear Conditioning Requires Protein Synthesis and Protein Kinase A in the Amygdala
599
Citations
29
References
2000
Year
NeuropsychologyBrain MechanismNeurolinguisticsInhibitory ProcessAffective NeuroscienceExplicit MemoryPsychologySocial SciencesProtein Kinase AAuditory Fear ConditioningMemoryCognitive NeuroscienceAuditory ProcessingCognitive ScienceMemory ConsolidationNeuropharmacologyPharmacologyNeurobiological MechanismNeurophysiologyNeurobiological FactorLong-term PotentiationProcedural MemoryNeuroscienceBiological PsychiatryBlock LtpMedicineAuditory System
Auditory fear conditioning induces long‑term potentiation‑like changes in the lateral amygdala, a region where LTP can be elicited by central auditory pathway stimulation. The study tested whether blocking protein synthesis or PKA activity in the lateral amygdala after conditioning disrupts consolidation of auditory fear memory. Rats received a single conditioning trial followed immediately by intra‑lateral‑amygdala infusions of anisomycin or Rp‑cAMPS, then were tested 24 h later. Immediate post‑training infusions of either drug dose‑dependently impaired long‑term fear memory while 6‑hour delayed infusions had no effect, indicating that the lateral amygdala’s consolidation of auditory fear depends on PKA‑mediated protein synthesis.
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.
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