Background:We recently reported experimental and theoretical evidence for a long-term mechanism that amplifies the response of a subset of neurons that were recruited during fear learning that was termed “memory amplification mechanism”. This mechanism is mediated CaMKII dependent twofold increase of the strength of all inhibitory and all excitatory synapses in the cell. The key function of the amplification mechanism is to promote an already-formed memory to a dominant memory.Aim:Using TRAP2 genetically modified mice, we investigated the long-term retention of traumatic memory through an amplification mechanism and target pharmacologically to modulate or suppress its effect.Methods:Fear conditioning was conducted for 2 consecutive days. Retrieval was performed over 8 weeks to assess long-term retention of the amplification mechanism. Miniature synaptic events were recorded via whole-cell patch clamp from neurons in the lateral amygdala of a transgenic mouse model expressing TRAP2/fos fluorescence cells after fear-memory retrieval. CaMKII competitive blocker was administered to investigate its effect on memory amplification. Results:Freezing persisted for 8 weeks post extensive training. Additionally, synaptic current amplitudes increased selectively in neurons tagged with TRAP2/fos after fear-memory retrieval. The CaMKII competitive blocker reduces freezing time indicating that the strength of the fear memory can be reduced by targeting CaMKII phosphorylation.Conclusion:Taken together, the dominant aversive memory is maintained by a sub-group of neurons on which all synaptic inputs, inhibitory and excitatory are doubled. The board strengthening is controlled by postsynaptic CaMKII-mediated enhanced channel conductance.