Document Detail


Protein synthesis inhibition and memory: formation vs amnesia.
MedLine Citation:
PMID:  18054504     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Studies using protein synthesis inhibitors have provided key support for the prevalent view that memory formation requires the initiation of protein synthesis as a primary element of the molecular biology of memory. However, many other interpretations of the amnesia data have received far less attention. These include: (a) protein synthesis may play a constitutive role in memory formation, providing proteins prior to an experience that can be activated by training; (b) protein synthesis may be needed to replace proteins available prior to learning but 'consumed' by learning; (c) inhibition of protein synthesis impairs the well-being of neurons, leading to an inability to deliver resources needed for memory formation; and (d) inhibition of protein synthesis results in abnormal neural functions that interfere with memory. One of these, abnormal release of neurotransmitters after inhibition of protein synthesis, is detailed here, along with a review of many circumstances in which it appears that protein synthesis at the time of training is not required for the formation of new memories. Evidence of activation of cell signaling molecules and transcription factors is another form of support for a role of training-initiated protein synthesis in memory. However, recent findings suggest that many of these molecules are activated by training and remain activated for days after training, i.e. activated for times well beyond those typically invoked for memory consolidation processes. Reviewing these results, this paper suggests that the long-lasting molecular changes may be the basis of a form of intracellular memory, one responsible for up-regulating the probability that a neuron, once activated in this manner, will engage in future plasticity. This view melds ideas of modulation of memory with those of consolidation of memory.
Authors:
Paul E Gold
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2007-12-03
Journal Detail:
Title:  Neurobiology of learning and memory     Volume:  89     ISSN:  1095-9564     ISO Abbreviation:  Neurobiol Learn Mem     Publication Date:  2008 Mar 
Date Detail:
Created Date:  2008-03-10     Completed Date:  2008-06-16     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  9508166     Medline TA:  Neurobiol Learn Mem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  201-11     Citation Subset:  IM    
Affiliation:
Department of Psychology and Psychiatry, Neuroscience Program and Institute for Genomic Biology, University of Illinois, 603 E. Daniel Street, Champaign, IL 61820, USA. pgold@uiuc.edu
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MeSH Terms
Descriptor/Qualifier:
Amnesia, Retrograde / chemically induced*,  physiopathology*
Amygdala / drug effects
Anisomycin / administration & dosage,  adverse effects*
Conditioning, Classical / physiology
Discrimination Learning / drug effects
Humans
Memory / drug effects*
Neuronal Plasticity / drug effects
Protein Biosynthesis / drug effects*
Protein Synthesis Inhibitors / administration & dosage,  adverse effects*
Serotonin / metabolism
Signal Transduction / drug effects
Grant Support
ID/Acronym/Agency:
AG007648/AG/NIA NIH HHS; DA016951/DA/NIDA NIH HHS; DA024129/DA/NIDA NIH HHS; R01 AG007648-17/AG/NIA NIH HHS; R01 DA016951-04/DA/NIDA NIH HHS; R21 DA024129-01/DA/NIDA NIH HHS
Chemical
Reg. No./Substance:
0/Protein Synthesis Inhibitors; 22862-76-6/Anisomycin; 50-67-9/Serotonin
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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