Abstract
Learning of new information is transformed into long-lasting memory through a process known as consolidation, which requires protein synthesis. Classical theory held that once consolidated, memory was insensitive to disruption. However, old memories that are insensitive to protein synthesis inhibitors can become vulnerable if they are recalled (reactivated). These findings led to a new hypothesis that when an old memory is reactivated, it again becomes labile and, similar to a newly formed memory, requires a process of reconsolidation in order to be maintained. Here, we show that the requirement for protein synthesis of a reactivated memory is evident only when the memory is recent. In fact, memory vulnerability decreases as the time between the original training and the recall increases.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amygdala / drug effects
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Amygdala / metabolism
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Animals
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Anisomycin / pharmacology
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Brain / drug effects
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Brain / metabolism*
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Hippocampus / drug effects
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Hippocampus / metabolism
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Learning / drug effects
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Learning / physiology*
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Male
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Memory / drug effects
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Memory / physiology*
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Memory Disorders / chemically induced
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Memory Disorders / metabolism*
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Memory Disorders / physiopathology
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Nerve Tissue Proteins / antagonists & inhibitors
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Nerve Tissue Proteins / biosynthesis*
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Neural Pathways / drug effects
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Neural Pathways / metabolism
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Protein Synthesis Inhibitors / pharmacology
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Rats
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Rats, Long-Evans
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Reaction Time / drug effects
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Reaction Time / physiology*
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Synapses / drug effects
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Synapses / metabolism
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Synaptic Transmission / drug effects
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Synaptic Transmission / physiology
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Time Factors
Substances
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Nerve Tissue Proteins
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Protein Synthesis Inhibitors
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Anisomycin