Long-term stability of fear memory depends on the synthesis of protein but not mRNA in the amygdala

Eur J Neurosci. 2006 Apr;23(7):1853-9. doi: 10.1111/j.1460-9568.2006.04723.x.


Synaptic modification supporting memory formation is thought to depend on gene expression and protein synthesis. Disrupting either process around the time of learning prevents the formation of long-term memory. Recent evidence suggests that memory also becomes susceptible to disruption upon retrieval. Whether or not the molecular events involved in the formation of new memory are the same as what is needed for memory to persist after retrieval has yet to be determined. In the present set of experiments, rats were given inhibitors of protein or messenger ribonucleic acid (mRNA) synthesis into the amygdala just after training or retrieval of fear memory. Results showed that blocking mRNA or protein synthesis immediately after learning prevented the formation of long-term memory, while stability of memory after retrieval required protein, but not mRNA, synthesis. These data suggest that the protein needed for memory reconsolidation after retrieval may be transcribed from pre-existing stores of mRNA.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Amygdala / drug effects
  • Amygdala / metabolism*
  • Animals
  • Anisomycin / pharmacology
  • Cerebrospinal Fluid
  • Dactinomycin / pharmacology
  • Dichlororibofuranosylbenzimidazole / pharmacology
  • Fear*
  • Male
  • Memory*
  • Protein Biosynthesis* / drug effects
  • Protein Synthesis Inhibitors / pharmacology
  • RNA, Messenger / antagonists & inhibitors
  • RNA, Messenger / biosynthesis*
  • Rats
  • Rats, Long-Evans
  • Time Factors


  • Protein Synthesis Inhibitors
  • RNA, Messenger
  • Dactinomycin
  • Dichlororibofuranosylbenzimidazole
  • Anisomycin