Translational control via the mammalian target of rapamycin pathway is critical for the formation and stability of long-term fear memory in amygdala neurons. J Neurosci 2006 Dec 13;26(50):12977-83
Date
12/15/2006Pubmed ID
17167087Pubmed Central ID
PMC6674972DOI
10.1523/JNEUROSCI.4209-06.2006Scopus ID
2-s2.0-33845606405 (requires institutional sign-in at Scopus site) 219 CitationsAbstract
The mammalian target of rapamycin kinase (mTOR) regulates protein synthesis in neurons at the translational level through phosphorylation of several intracellular targets. Recent work in invertebrates indicates that mTOR-dependent translational control may be critical for the induction and maintenance of activity-dependent synaptic plasticity underlying memory formation. Here, we report that training rats in a simple fear conditioning procedure evokes a time-dependent increase in the phosphorylation of p70s6 kinase, a major direct downstream target of mTOR. When the activation of mTOR was prevented by posttraining injection of rapamycin into the amygdala, formation of the memory and the increase in p70s6 kinase phosphorylation was attenuated. Furthermore, when rapamycin was applied to the amygdala after the recall of a previously stored fear memory, subsequent retention was disrupted, indicating that local translational control at active synapses is required for the stability as well as the formation of long-term memory in this system.
Author List
Parsons RG, Gafford GM, 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
Acoustic StimulationAmygdala
Animals
Fear
Injections, Intraventricular
Male
Memory
Neurons
Protein Biosynthesis
Protein Kinases
Rats
Rats, Long-Evans
Ribosomal Protein S6 Kinases, 70-kDa
Sirolimus
TOR Serine-Threonine Kinases
Time Factors
