Properties of Contextual Memory Formed in the Absence of αCaMKII Autophosphorylation

<p>Abstract</p> <p>The alpha-isoform of calcium/calmodulin-dependent kinase II (αCaMKII) is a major synaptic kinase that undergoes autophosphorylation after NMDA receptor activation, switching the kinase into a calcium-independent activity state. This αCaMKII autophosphorylation is...

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Main Authors: Irvine Elaine E, Danhiez Arthur, Radwanska Kasia, Nassim Charlotte, Lucchesi Walter, Godaux Emile, Ris Laurence, Giese K
Format: Article
Language:English
Published: BMC 2011-01-01
Series:Molecular Brain
Online Access:http://www.molecularbrain.com/content/4/1/8
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spelling doaj-a306113ea5c44cf89221251662d133de2020-11-24T21:20:19ZengBMCMolecular Brain1756-66062011-01-0141810.1186/1756-6606-4-8Properties of Contextual Memory Formed in the Absence of αCaMKII AutophosphorylationIrvine Elaine EDanhiez ArthurRadwanska KasiaNassim CharlotteLucchesi WalterGodaux EmileRis LaurenceGiese K<p>Abstract</p> <p>The alpha-isoform of calcium/calmodulin-dependent kinase II (αCaMKII) is a major synaptic kinase that undergoes autophosphorylation after NMDA receptor activation, switching the kinase into a calcium-independent activity state. This αCaMKII autophosphorylation is essential for NMDA receptor-dependent long-term potentiation (LTP), induced by a single tetanus, in hippocampal area CA1 and in neocortex. Furthermore, the αCaMKII autophosphorylation is essential for contextual long-term memory (LTM) formation after a single training trial but not after a massed training session. Here, we show that in the absence of αCaMKII autophosphorylation contextual fear conditioning is hippocampus dependent and that multi-tetanus-dependent late-LTP cannot be induced in hippocampal area CA1. Furthermore, we show that in the absence of αCaMKII autophosphorylation contextual LTM persists for 30 days, the latest time point tested. Additionally, contextual, but not cued, LTM formation in the absence of αCaMKII autophosphorylation appears to be impaired in 18 month-old mice. Taken together, our findings suggest that αCaMKII autophosphorylation-independent plasticity in the hippocampus is sufficient for contextual LTM formation and that αCaMKII autophosphorylation may be important for delaying age-related impairments in hippocampal memory formation. Furthermore, they propose that NMDA receptor-dependent LTP in hippocampal area CA1 is essential for contextual LTM formation after a single trial but not after massed training. Finally, our results challenge the proposal that NMDA receptor-dependent LTP in neocortex is required for remote contextual LTM.</p> http://www.molecularbrain.com/content/4/1/8
collection DOAJ
language English
format Article
sources DOAJ
author Irvine Elaine E
Danhiez Arthur
Radwanska Kasia
Nassim Charlotte
Lucchesi Walter
Godaux Emile
Ris Laurence
Giese K
spellingShingle Irvine Elaine E
Danhiez Arthur
Radwanska Kasia
Nassim Charlotte
Lucchesi Walter
Godaux Emile
Ris Laurence
Giese K
Properties of Contextual Memory Formed in the Absence of αCaMKII Autophosphorylation
Molecular Brain
author_facet Irvine Elaine E
Danhiez Arthur
Radwanska Kasia
Nassim Charlotte
Lucchesi Walter
Godaux Emile
Ris Laurence
Giese K
author_sort Irvine Elaine E
title Properties of Contextual Memory Formed in the Absence of αCaMKII Autophosphorylation
title_short Properties of Contextual Memory Formed in the Absence of αCaMKII Autophosphorylation
title_full Properties of Contextual Memory Formed in the Absence of αCaMKII Autophosphorylation
title_fullStr Properties of Contextual Memory Formed in the Absence of αCaMKII Autophosphorylation
title_full_unstemmed Properties of Contextual Memory Formed in the Absence of αCaMKII Autophosphorylation
title_sort properties of contextual memory formed in the absence of αcamkii autophosphorylation
publisher BMC
series Molecular Brain
issn 1756-6606
publishDate 2011-01-01
description <p>Abstract</p> <p>The alpha-isoform of calcium/calmodulin-dependent kinase II (αCaMKII) is a major synaptic kinase that undergoes autophosphorylation after NMDA receptor activation, switching the kinase into a calcium-independent activity state. This αCaMKII autophosphorylation is essential for NMDA receptor-dependent long-term potentiation (LTP), induced by a single tetanus, in hippocampal area CA1 and in neocortex. Furthermore, the αCaMKII autophosphorylation is essential for contextual long-term memory (LTM) formation after a single training trial but not after a massed training session. Here, we show that in the absence of αCaMKII autophosphorylation contextual fear conditioning is hippocampus dependent and that multi-tetanus-dependent late-LTP cannot be induced in hippocampal area CA1. Furthermore, we show that in the absence of αCaMKII autophosphorylation contextual LTM persists for 30 days, the latest time point tested. Additionally, contextual, but not cued, LTM formation in the absence of αCaMKII autophosphorylation appears to be impaired in 18 month-old mice. Taken together, our findings suggest that αCaMKII autophosphorylation-independent plasticity in the hippocampus is sufficient for contextual LTM formation and that αCaMKII autophosphorylation may be important for delaying age-related impairments in hippocampal memory formation. Furthermore, they propose that NMDA receptor-dependent LTP in hippocampal area CA1 is essential for contextual LTM formation after a single trial but not after massed training. Finally, our results challenge the proposal that NMDA receptor-dependent LTP in neocortex is required for remote contextual LTM.</p>
url http://www.molecularbrain.com/content/4/1/8
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