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
Date
04/21/2006Pubmed ID
16623842Pubmed Central ID
PMC1698267DOI
10.1111/j.1460-9568.2006.04723.xScopus ID
2-s2.0-33645451289 (requires institutional sign-in at Scopus site) 80 CitationsAbstract
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.
Author List
Parsons RG, Gafford GM, Baruch DE, Riedner BA, Helmstetter FJAuthor
Fred Helmstetter PhD Professor in the Psychology / Neuroscience department at University of Wisconsin - MilwaukeeMESH terms used to index this publication - Major topics in bold
AmygdalaAnimals
Anisomycin
Cerebrospinal Fluid
Dactinomycin
Dichlororibofuranosylbenzimidazole
Fear
Male
Memory
Protein Biosynthesis
Protein Synthesis Inhibitors
RNA, Messenger
Rats
Rats, Long-Evans
Time Factors
