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GluR2 endocytosis-dependent protein degradation in the amygdala mediates memory updating

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dc.contributor.authorFerrara, Nicole C.en
dc.contributor.authorJarome, Timothy J.en
dc.contributor.authorCullen, Patrick K.en
dc.contributor.authorOrsi, Sabrina A.en
dc.contributor.authorKwapis, Janine L.en
dc.contributor.authorTrask, Sydneyen
dc.contributor.authorPullins, Shane E.en
dc.contributor.authorHelmstetter, Fred J.en
dc.contributor.departmentAnimal and Poultry Sciencesen
dc.contributor.departmentSchool of Neuroscienceen
dc.date.accessioned2019-07-23T16:50:04Zen
dc.date.available2019-07-23T16:50:04Zen
dc.date.issued2019-03-26en
dc.description.abstractAssociations learned during Pavlovian fear conditioning are rapidly acquired and long lasting, providing an ideal model for studying long-term memory formation, storage, and retrieval. During retrieval, these memories can "destabilize" and become labile, allowing a transient "reconsolidation" window during which the memory can be updated, suggesting that reconsolidation could be an attractive target for the modification of memories related to past traumatic experiences. This memory destabilization process is regulated by protein degradation and GluR2-endocytosis in the amygdala. However, it is currently unknown if retrieval-dependent GluR2-endocytosis in the amygdala is critical for incorporation of new information into the memory trace. We examined whether the addition of new information during memory retrieval required GluR2-endocytosis to modify the original memory. The presentation of two foot shocks of weaker intensity during retrieval resulted in GluR2 endocytosis-dependent increase in fear responding on a later test, suggesting modification of the original memory. This increase in fear expression was associated with increased protein degradation and zif268 expression in the same population of cells in the amygdala, indicating increased destabilization processes and cellular activity, and both were lost following blockade of GluR2-endocytosis. These data suggest that the endocytosis of GluR2-containing AMPA receptors in the amygdala regulates retrieval-induced strengthening of memories for traumatic events by modulating cellular destabilization and activity.en
dc.description.notesThis work was supported by National Institute of Health (NIH) grants MH112141 and AG053854 (FJH) and startup funds from the College of Agricultural and Life Sciences and the College of Science at Virginia Tech (TJJ).en
dc.description.sponsorshipNational Institute of Health (NIH) [MH112141, AG053854]en
dc.description.sponsorshipCollege of Agricultural and Life Sciencesen
dc.description.sponsorshipCollege of Science at Virginia Techen
dc.format.mimetypeapplication/pdfen
dc.identifier.doihttps://doi.org/10.1038/s41598-019-41526-1en
dc.identifier.issn2045-2322en
dc.identifier.other5180en
dc.identifier.pmid30914678en
dc.identifier.urihttp://hdl.handle.net/10919/91925en
dc.identifier.volume9en
dc.language.isoenen
dc.publisherSpringer Natureen
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.subjectubiquitin-proteasome systemen
dc.subjectfear memoryen
dc.subjectucs revaluationen
dc.subjectcontext fearen
dc.subjectreconsolidationen
dc.subjectretrievalen
dc.subjectreceptoren
dc.subjectdestabilizationen
dc.subjectconsolidationen
dc.subjecthippocampusen
dc.titleGluR2 endocytosis-dependent protein degradation in the amygdala mediates memory updatingen
dc.title.serialScientific Reportsen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten
dc.type.dcmitypeStillImageen

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