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An endogenous inhibitor of calcium/calmodulin‐dependent kinase II is up‐regulated during consolidation of fear memory
Author(s) -
Lepicard Eve M.,
Mizuno Keiko,
AntunesMartins Ana,
Von Hertzen Laura S. J.,
Giese K. Peter
Publication year - 2006
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2006.04830.x
Subject(s) - dentate gyrus , memory consolidation , hippocampal formation , endogeny , fear conditioning , hippocampus , amygdala , in situ hybridization , long term potentiation , calmodulin , neuroscience , biology , gene expression , microbiology and biotechnology , chemistry , endocrinology , gene , receptor , biochemistry , enzyme
CaMKIINα and CaMKIINβ are endogenous inhibitors of the abundant synaptic protein, calcium/calmodulin‐dependent protein kinase II (CaMKII). CaMKII exerts a prominent function in memory formation and the endogenous inhibitors might be important regulators of CaMKII activity during this process. Here we investigated whether or not CaMKIINα and CaMKIINβ gene expressions are regulated in the mouse hippocampus and amygdala after background contextual fear conditioning. Quantitative real‐time PCR revealed that the hippocampal expression of CaMKIINα mRNA was up‐regulated 30 and 60 min after conditioning. In contrast, CaMKIINβ mRNA expression did not change. The up‐regulation of CaMKIINα expression was specific for the fear memory because the context alone and a shock control did not induce any variation of transcription level. Quantification of in situ hybridization signals showed that CaMKIINα expression increased in hippocampal area CA1, in the dentate gyrus (DG) and in the lateral amygdala (LA) 30 min after training. Our findings show an up‐regulation in the expression of the endogenous inhibitor gene CaMKIINα during consolidation of fear memory. The early onset and the amplitude of the up‐regulation are similar to those of immediate‐early genes. Taken together, our results suggest that the CaMKIINα inhibitor has a physiological role in controlling CaMKII activity from an early stage of memory consolidation.