Interactions between the amygdala and medial prefrontal cortex as upstream regulators of the hippocampus to reconsolidate and enhance retrieved inhibitory avoidance memory
Abstract Memory reconsolidation is thought to maintain or enhance an original memory or add new information to the memory. Retrieved inhibitory avoidance (IA) memory is enhanced through memory reconsolidation by activating gene expression in the amygdala, medial prefrontal cortex (mPFC), and hippoca...
| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
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BMC
2021-03-01
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| Series: | Molecular Brain |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s13041-021-00753-2 |
| _version_ | 1818574563647160320 |
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| author | Hotaka Fukushima Yue Zhang Satoshi Kida |
| author_facet | Hotaka Fukushima Yue Zhang Satoshi Kida |
| author_sort | Hotaka Fukushima |
| collection | DOAJ |
| description | Abstract Memory reconsolidation is thought to maintain or enhance an original memory or add new information to the memory. Retrieved inhibitory avoidance (IA) memory is enhanced through memory reconsolidation by activating gene expression in the amygdala, medial prefrontal cortex (mPFC), and hippocampus. However, it remains unclear how these regions interact to reconsolidate/enhance IA memory. Here, we found the interactions between the amygdala and mPFC as upstream regulators of the hippocampus for IA memory reconsolidation. Pharmacological inactivation of the amygdala, mPFC, or hippocampus immediately after IA memory retrieval blocked IA memory enhancement. More importantly, inactivation of the amygdala or mPFC blocked the induction of c-Fos in the amygdala, mPFC, and hippocampus, whereas hippocampal blockade inhibited it only in the hippocampus. These observations suggest interactions between the amygdala and mPFC and they both function as upstream regulators of the hippocampus to reconsolidate IA memory. Our findings suggest circuitry mechanisms underlying IA memory enhancement through reconsolidation between the amygdala, mPFC, and hippocampus. |
| first_indexed | 2024-12-15T00:28:13Z |
| format | Article |
| id | doaj.art-dafaa863fc9349a0b0ef2540c69f0a94 |
| institution | Directory Open Access Journal |
| issn | 1756-6606 |
| language | English |
| last_indexed | 2024-12-15T00:28:13Z |
| publishDate | 2021-03-01 |
| publisher | BMC |
| record_format | Article |
| series | Molecular Brain |
| spelling | doaj.art-dafaa863fc9349a0b0ef2540c69f0a942022-12-21T22:42:07ZengBMCMolecular Brain1756-66062021-03-011411510.1186/s13041-021-00753-2Interactions between the amygdala and medial prefrontal cortex as upstream regulators of the hippocampus to reconsolidate and enhance retrieved inhibitory avoidance memoryHotaka Fukushima0Yue Zhang1Satoshi Kida2Department of Bioscience, Faculty of Life Sciences, Tokyo University of AgricultureDepartment of Bioscience, Faculty of Life Sciences, Tokyo University of AgricultureDepartment of Bioscience, Faculty of Life Sciences, Tokyo University of AgricultureAbstract Memory reconsolidation is thought to maintain or enhance an original memory or add new information to the memory. Retrieved inhibitory avoidance (IA) memory is enhanced through memory reconsolidation by activating gene expression in the amygdala, medial prefrontal cortex (mPFC), and hippocampus. However, it remains unclear how these regions interact to reconsolidate/enhance IA memory. Here, we found the interactions between the amygdala and mPFC as upstream regulators of the hippocampus for IA memory reconsolidation. Pharmacological inactivation of the amygdala, mPFC, or hippocampus immediately after IA memory retrieval blocked IA memory enhancement. More importantly, inactivation of the amygdala or mPFC blocked the induction of c-Fos in the amygdala, mPFC, and hippocampus, whereas hippocampal blockade inhibited it only in the hippocampus. These observations suggest interactions between the amygdala and mPFC and they both function as upstream regulators of the hippocampus to reconsolidate IA memory. Our findings suggest circuitry mechanisms underlying IA memory enhancement through reconsolidation between the amygdala, mPFC, and hippocampus.https://doi.org/10.1186/s13041-021-00753-2Memory reconsolidationAmygdalaMedial prefrontal cortexHippocampusMemory retrievalMemory enhancement |
| spellingShingle | Hotaka Fukushima Yue Zhang Satoshi Kida Interactions between the amygdala and medial prefrontal cortex as upstream regulators of the hippocampus to reconsolidate and enhance retrieved inhibitory avoidance memory Molecular Brain Memory reconsolidation Amygdala Medial prefrontal cortex Hippocampus Memory retrieval Memory enhancement |
| title | Interactions between the amygdala and medial prefrontal cortex as upstream regulators of the hippocampus to reconsolidate and enhance retrieved inhibitory avoidance memory |
| title_full | Interactions between the amygdala and medial prefrontal cortex as upstream regulators of the hippocampus to reconsolidate and enhance retrieved inhibitory avoidance memory |
| title_fullStr | Interactions between the amygdala and medial prefrontal cortex as upstream regulators of the hippocampus to reconsolidate and enhance retrieved inhibitory avoidance memory |
| title_full_unstemmed | Interactions between the amygdala and medial prefrontal cortex as upstream regulators of the hippocampus to reconsolidate and enhance retrieved inhibitory avoidance memory |
| title_short | Interactions between the amygdala and medial prefrontal cortex as upstream regulators of the hippocampus to reconsolidate and enhance retrieved inhibitory avoidance memory |
| title_sort | interactions between the amygdala and medial prefrontal cortex as upstream regulators of the hippocampus to reconsolidate and enhance retrieved inhibitory avoidance memory |
| topic | Memory reconsolidation Amygdala Medial prefrontal cortex Hippocampus Memory retrieval Memory enhancement |
| url | https://doi.org/10.1186/s13041-021-00753-2 |
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