NMDA receptors are critical for unleashing consolidated auditory fear memories.

Memories are dynamic and can change when recalled. The process that returns memories to a labile state during remembering is unclear. We found that the presence of NMDA, but not AMPA, receptor antagonists in the amygdala prior to recall prevented the consolidated fear memory from returning to a labile state.

Extinction is not a sufficient condition to prevent fear memories from undergoing reconsolidation in the basolateral amygdala.

Consolidated memories when reactivated may return to a state that requires protein synthesis in order to be restabilized (reconsolidation). It has been shown in a variety of systems that if reactivation induces significant extinction then extinction is the protein synthesis dependent memory state, rather than reconsolidation. Thus, extinction consolidation may prevent the memory from undergoing reconsolidation.

Translational control of hippocampal synaptic plasticity and memory by the eIF2alpha kinase GCN2.

Studies on various forms of synaptic plasticity have shown a link between messenger RNA translation, learning and memory. Like memory, synaptic plasticity includes an early phase that depends on modification of pre-existing proteins, and a late phase that requires transcription and synthesis of new proteins. Activation of postsynaptic targets seems to trigger the transcription of plasticity-related genes.