Lack of drug-induced post-retrieval amnesia for auditory fear memories in rats

Abstract Background Long-term memory formation is generally assumed to involve the permanent storage of recently acquired memories, making them relatively insensitive disruption, a process referred as consolidation. However, when retrieved under specific circumstances, consolidated fear memories are thought return labile state, thereby opening window for modification (e.g., attenuation) memory. Several interventions during critical time frame after this destabilization seem be able alter memory, example by pharmacologically interfering with restabilization process, either direct protein synthesis inhibition or indirectly, using drugs that can safely administered in patients propranolol). Here, we find that, contrary expectations, systemic pharmacological manipulations auditory fear-conditioned rats do not lead drug-induced post-retrieval amnesia. Results In series well-powered conditioning experiments (four propranolol, 10 mg/kg, two rapamycin, 20–40 one anisomycin, 150 mg/kg and cycloheximide, 1.5 mg/kg), found no evidence reduced cued expression drug-free test adult male Sprague-Dawley had previously received drug injection upon retrieval tone All used standard reactivation procedures freezing behavioral read-out (conceptual exact replications published reports) common agents. Additional tests confirmed applied doses administration routes were effective inducing their conventional effects on (propranolol, acutely), body weight (rapamycin, cycloheximide), consolidation extinction (cycloheximide). Conclusions contrast studies, did amnesia, underlining effect, well its clinical applicability, may considerably more constrained less readily reproduced than what current literature would suggest.