Activity dependent protein degradation is critical for the formation and stability of fear memory in the amygdala.

Protein degradation through the ubiquitin-proteasome system [UPS] plays a critical role in some forms of synaptic plasticity. However, its role in memory formation in the amygdala, a site critical for the formation of fear memories, currently remains unknown. Here we provide the first evidence that...

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Autores principales:	Timothy J Jarome, Craig T Werner, Janine L Kwapis, Fred J Helmstetter
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/03e78f20d63946e699dc6037aa7c59d5
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id	oai:doaj.org-article:03e78f20d63946e699dc6037aa7c59d5
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spelling	oai:doaj.org-article:03e78f20d63946e699dc6037aa7c59d52021-11-04T06:08:05ZActivity dependent protein degradation is critical for the formation and stability of fear memory in the amygdala.1932-620310.1371/journal.pone.0024349https://doaj.org/article/03e78f20d63946e699dc6037aa7c59d52011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21961035/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Protein degradation through the ubiquitin-proteasome system [UPS] plays a critical role in some forms of synaptic plasticity. However, its role in memory formation in the amygdala, a site critical for the formation of fear memories, currently remains unknown. Here we provide the first evidence that protein degradation through the UPS is critically engaged at amygdala synapses during memory formation and retrieval. Fear conditioning results in NMDA-dependent increases in degradation-specific polyubiquitination in the amygdala, targeting proteins involved in translational control and synaptic structure and blocking the degradation of these proteins significantly impairs long-term memory. Furthermore, retrieval of fear memory results in a second wave of NMDA-dependent polyubiquitination that targets proteins involved in translational silencing and synaptic structure and is critical for memory updating following recall. These results indicate that UPS-mediated protein degradation is a major regulator of synaptic plasticity necessary for the formation and stability of long-term memories at amygdala synapses.Timothy J JaromeCraig T WernerJanine L KwapisFred J HelmstetterPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 9, p e24349 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Timothy J Jarome Craig T Werner Janine L Kwapis Fred J Helmstetter Activity dependent protein degradation is critical for the formation and stability of fear memory in the amygdala.
description	Protein degradation through the ubiquitin-proteasome system [UPS] plays a critical role in some forms of synaptic plasticity. However, its role in memory formation in the amygdala, a site critical for the formation of fear memories, currently remains unknown. Here we provide the first evidence that protein degradation through the UPS is critically engaged at amygdala synapses during memory formation and retrieval. Fear conditioning results in NMDA-dependent increases in degradation-specific polyubiquitination in the amygdala, targeting proteins involved in translational control and synaptic structure and blocking the degradation of these proteins significantly impairs long-term memory. Furthermore, retrieval of fear memory results in a second wave of NMDA-dependent polyubiquitination that targets proteins involved in translational silencing and synaptic structure and is critical for memory updating following recall. These results indicate that UPS-mediated protein degradation is a major regulator of synaptic plasticity necessary for the formation and stability of long-term memories at amygdala synapses.
format	article
author	Timothy J Jarome Craig T Werner Janine L Kwapis Fred J Helmstetter
author_facet	Timothy J Jarome Craig T Werner Janine L Kwapis Fred J Helmstetter
author_sort	Timothy J Jarome
title	Activity dependent protein degradation is critical for the formation and stability of fear memory in the amygdala.
title_short	Activity dependent protein degradation is critical for the formation and stability of fear memory in the amygdala.
title_full	Activity dependent protein degradation is critical for the formation and stability of fear memory in the amygdala.
title_fullStr	Activity dependent protein degradation is critical for the formation and stability of fear memory in the amygdala.
title_full_unstemmed	Activity dependent protein degradation is critical for the formation and stability of fear memory in the amygdala.
title_sort	activity dependent protein degradation is critical for the formation and stability of fear memory in the amygdala.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/03e78f20d63946e699dc6037aa7c59d5
work_keys_str_mv	AT timothyjjarome activitydependentproteindegradationiscriticalfortheformationandstabilityoffearmemoryintheamygdala AT craigtwerner activitydependentproteindegradationiscriticalfortheformationandstabilityoffearmemoryintheamygdala AT janinelkwapis activitydependentproteindegradationiscriticalfortheformationandstabilityoffearmemoryintheamygdala AT fredjhelmstetter activitydependentproteindegradationiscriticalfortheformationandstabilityoffearmemoryintheamygdala
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Activity dependent protein degradation is critical for the formation and stability of fear memory in the amygdala.

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