Prevention of long-term memory loss after retrieval by an endogenous CaMKII inhibitor

Abstract CaMK2N1 and CaMK2N2 are endogenous inhibitors of calcium/calmodulin-dependent protein kinase II (CaMKII), a key synaptic signaling molecule for learning and memory. Here, we investigated the learning and memory function of CaMK2N1 by knocking-down its expression in dorsal hippocampus of mic...

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Autores principales:	Fabio Antonio Vigil, Keiko Mizuno, Walter Lucchesi, Victoria Valls-Comamala, Karl Peter Giese
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/bc2e7ec7e3ff46f7aa216e6251ca56ce
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spelling	oai:doaj.org-article:bc2e7ec7e3ff46f7aa216e6251ca56ce2021-12-02T16:06:19ZPrevention of long-term memory loss after retrieval by an endogenous CaMKII inhibitor10.1038/s41598-017-04355-82045-2322https://doaj.org/article/bc2e7ec7e3ff46f7aa216e6251ca56ce2017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-04355-8https://doaj.org/toc/2045-2322Abstract CaMK2N1 and CaMK2N2 are endogenous inhibitors of calcium/calmodulin-dependent protein kinase II (CaMKII), a key synaptic signaling molecule for learning and memory. Here, we investigated the learning and memory function of CaMK2N1 by knocking-down its expression in dorsal hippocampus of mice. We found that reduced CaMK2N1 expression does not affect contextual fear long-term memory (LTM) formation. However, we show that it impairs maintenance of established LTM, but only if retrieval occurs. CaMK2N1 knockdown prevents a decrease of threonine-286 (T286) autophosphorylation of αCaMKII and increases GluA1 levels in hippocampal synapses after retrieval of contextual fear LTM. CaMK2N1 knockdown can also increase CaMK2N2 expression, but we show that such increased expression does not affect LTM after retrieval. We also found that substantial overexpression of CaMK2N2 in dorsal hippocampus impairs LTM formation, but not LTM maintenance, suggesting that CaMKII activity is not required for LTM storage. Taken together, we propose a specific function for CaMK2N1; enabling LTM maintenance after retrieval by inhibiting T286 autophosphorylation of αCaMKII.Fabio Antonio VigilKeiko MizunoWalter LucchesiVictoria Valls-ComamalaKarl Peter GieseNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-9 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Fabio Antonio Vigil Keiko Mizuno Walter Lucchesi Victoria Valls-Comamala Karl Peter Giese Prevention of long-term memory loss after retrieval by an endogenous CaMKII inhibitor
description	Abstract CaMK2N1 and CaMK2N2 are endogenous inhibitors of calcium/calmodulin-dependent protein kinase II (CaMKII), a key synaptic signaling molecule for learning and memory. Here, we investigated the learning and memory function of CaMK2N1 by knocking-down its expression in dorsal hippocampus of mice. We found that reduced CaMK2N1 expression does not affect contextual fear long-term memory (LTM) formation. However, we show that it impairs maintenance of established LTM, but only if retrieval occurs. CaMK2N1 knockdown prevents a decrease of threonine-286 (T286) autophosphorylation of αCaMKII and increases GluA1 levels in hippocampal synapses after retrieval of contextual fear LTM. CaMK2N1 knockdown can also increase CaMK2N2 expression, but we show that such increased expression does not affect LTM after retrieval. We also found that substantial overexpression of CaMK2N2 in dorsal hippocampus impairs LTM formation, but not LTM maintenance, suggesting that CaMKII activity is not required for LTM storage. Taken together, we propose a specific function for CaMK2N1; enabling LTM maintenance after retrieval by inhibiting T286 autophosphorylation of αCaMKII.
format	article
author	Fabio Antonio Vigil Keiko Mizuno Walter Lucchesi Victoria Valls-Comamala Karl Peter Giese
author_facet	Fabio Antonio Vigil Keiko Mizuno Walter Lucchesi Victoria Valls-Comamala Karl Peter Giese
author_sort	Fabio Antonio Vigil
title	Prevention of long-term memory loss after retrieval by an endogenous CaMKII inhibitor
title_short	Prevention of long-term memory loss after retrieval by an endogenous CaMKII inhibitor
title_full	Prevention of long-term memory loss after retrieval by an endogenous CaMKII inhibitor
title_fullStr	Prevention of long-term memory loss after retrieval by an endogenous CaMKII inhibitor
title_full_unstemmed	Prevention of long-term memory loss after retrieval by an endogenous CaMKII inhibitor
title_sort	prevention of long-term memory loss after retrieval by an endogenous camkii inhibitor
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/bc2e7ec7e3ff46f7aa216e6251ca56ce
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Prevention of long-term memory loss after retrieval by an endogenous CaMKII inhibitor

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