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Inhibition of prefrontal protein synthesis following recall does not disrupt memory for trace fear conditioning

BACKGROUND: The extent of similarity between consolidation and reconsolidation is not yet fully understood. One of the differences noted is that not every brain region involved in consolidation exhibits reconsolidation. In trace fear conditioning, the hippocampus and the medial prefrontal cortex (mP...

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Autores principales: Blum, Sonja, Runyan, Jason D, Dash, Pramod K
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1617114/
https://www.ncbi.nlm.nih.gov/pubmed/17026758
http://dx.doi.org/10.1186/1471-2202-7-67
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author Blum, Sonja
Runyan, Jason D
Dash, Pramod K
author_facet Blum, Sonja
Runyan, Jason D
Dash, Pramod K
author_sort Blum, Sonja
collection PubMed
description BACKGROUND: The extent of similarity between consolidation and reconsolidation is not yet fully understood. One of the differences noted is that not every brain region involved in consolidation exhibits reconsolidation. In trace fear conditioning, the hippocampus and the medial prefrontal cortex (mPFC) are required for consolidation of long-term memory. We have previously demonstrated that trace fear memory is susceptible to infusion of the protein synthesis inhibitor anisomycin into the hippocampus following recall. In the present study, we examine whether protein synthesis inhibition in the mPFC following recall similarly results in the observation of reconsolidation of trace fear memory. RESULTS: Targeted intra-mPFC infusions of anisomycin or vehicle were performed immediately following recall of trace fear memory at 24 hours, or at 30 days, following training in a one-day or a two-day protocol. The present study demonstrates three key findings: 1) trace fear memory does not undergo protein synthesis dependent reconsolidation in the PFC, regardless of the intensity of the training, and 2) regardless of whether the memory is recent or remote, and 3) intra-mPFC inhibition of protein synthesis immediately following training impaired remote (30 days) memory. CONCLUSION: These results suggest that not all structures that participate in memory storage are involved in reconsolidation. Alternatively, certain types of memory-related information may reconsolidate, while other components of memory may not.
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spelling pubmed-16171142006-10-19 Inhibition of prefrontal protein synthesis following recall does not disrupt memory for trace fear conditioning Blum, Sonja Runyan, Jason D Dash, Pramod K BMC Neurosci Research Article BACKGROUND: The extent of similarity between consolidation and reconsolidation is not yet fully understood. One of the differences noted is that not every brain region involved in consolidation exhibits reconsolidation. In trace fear conditioning, the hippocampus and the medial prefrontal cortex (mPFC) are required for consolidation of long-term memory. We have previously demonstrated that trace fear memory is susceptible to infusion of the protein synthesis inhibitor anisomycin into the hippocampus following recall. In the present study, we examine whether protein synthesis inhibition in the mPFC following recall similarly results in the observation of reconsolidation of trace fear memory. RESULTS: Targeted intra-mPFC infusions of anisomycin or vehicle were performed immediately following recall of trace fear memory at 24 hours, or at 30 days, following training in a one-day or a two-day protocol. The present study demonstrates three key findings: 1) trace fear memory does not undergo protein synthesis dependent reconsolidation in the PFC, regardless of the intensity of the training, and 2) regardless of whether the memory is recent or remote, and 3) intra-mPFC inhibition of protein synthesis immediately following training impaired remote (30 days) memory. CONCLUSION: These results suggest that not all structures that participate in memory storage are involved in reconsolidation. Alternatively, certain types of memory-related information may reconsolidate, while other components of memory may not. BioMed Central 2006-10-06 /pmc/articles/PMC1617114/ /pubmed/17026758 http://dx.doi.org/10.1186/1471-2202-7-67 Text en Copyright © 2006 Blum et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Blum, Sonja
Runyan, Jason D
Dash, Pramod K
Inhibition of prefrontal protein synthesis following recall does not disrupt memory for trace fear conditioning
title Inhibition of prefrontal protein synthesis following recall does not disrupt memory for trace fear conditioning
title_full Inhibition of prefrontal protein synthesis following recall does not disrupt memory for trace fear conditioning
title_fullStr Inhibition of prefrontal protein synthesis following recall does not disrupt memory for trace fear conditioning
title_full_unstemmed Inhibition of prefrontal protein synthesis following recall does not disrupt memory for trace fear conditioning
title_short Inhibition of prefrontal protein synthesis following recall does not disrupt memory for trace fear conditioning
title_sort inhibition of prefrontal protein synthesis following recall does not disrupt memory for trace fear conditioning
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1617114/
https://www.ncbi.nlm.nih.gov/pubmed/17026758
http://dx.doi.org/10.1186/1471-2202-7-67
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