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Amygdala or hippocampus inactivation after retrieval induces temporary memory deficit

The hypothesis that memory is stored through a single stage of consolidation that results in a stable and lasting long-term memory has been challenged by the proposition that reactivation of a memory induces reconsolidation of the memory. The reconsolidation hypothesis is supported by evidence that,...

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Bibliographic Details
Published in:Neurobiology of learning and memory 2006-09, Vol.86 (2), p.144-149
Main Authors: Prado-Alcalá, Roberto A., Díaz del Guante, Miguel A., Garín-Aguilar, María E., Díaz-Trujillo, Arnulfo, Quirarte, Gina L., McGaugh, James L.
Format: Article
Language:English
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Summary:The hypothesis that memory is stored through a single stage of consolidation that results in a stable and lasting long-term memory has been challenged by the proposition that reactivation of a memory induces reconsolidation of the memory. The reconsolidation hypothesis is supported by evidence that, under some conditions, post-retrieval treatments affecting amygdala and hippocampus functioning impair subsequent retention performance. We now report that repeated retention testing attenuates the performance impairment induced by post-retrieval reversible inactivation of the amygdala and hippocampus of rats induced by tetrodotoxin. These findings challenge the reconsolidation hypothesis and suggest that the post-retrieval retention performance impairment is best explained as due to temporary retrieval failure.
ISSN:1074-7427
1095-9564
DOI:10.1016/j.nlm.2006.01.006