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Hippocampus. 2008;18(6):584-601. doi: 10.1002/hipo.20420.

A synaptic reinforcement-based model for transient amnesia following disruptions of memory consolidation and reconsolidation.

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Department of Biochemistry, Institute for Basic Health Sciences, Federal University of Rio Grande do Sul. Porto Alegre, RS, Brazil.


The observation of memory recovery following post-training amnestic interventions has historically caused controversy over the meaning of this finding, leading some authors to question the paradigm of a consolidation period for memories. Similarly, recent demonstrations of transient amnesia caused by interventions following memory reactivation have been used to question the existence of a retrieval-driven reconsolidation process. The present work aims to approach the phenomenon of transient amnesia following disruptions of consolidation and reconsolidation, discussing how memory recovery might be explained within a framework of systems consolidation, persistent synaptic reinforcement, and multiple memory traces. With these concepts in mind, we propose that long-term consolidation processes can underlie recovery from amnesia, demonstrating the feasibility of such a hypothesis in a two-structure computational model of learning in which consolidation is dependent upon synaptic reentry reinforcement. On the basis of this, we suggest that prolonged consolidation can account for experimental findings of transient amnesia, in a way that explains differences between disruptions of consolidation and reconsolidation without the need to dwell into the discussion between storage- and retrieval-based explanations for memory impairment.

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