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Differential regulation of CaMKII inhibitor beta protein expression after exposure to a novel context and during contextual fear memory formation.

Abstract:
Understanding of the molecular basis of long-term fear memory (fear LTM) formation provides targets in the treatment of emotional disorders. Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is one of the key synaptic molecules involved in fear LTM formation. There are two endogenous inhibitor proteins of CaMKII, CaMKII N alpha and N beta, which can regulate CaMKII activity in vitro. However, the physiological role of these endogenous inhibitors is not known. Here, we have investigated whether CaMKII N beta protein expression is regulated after contextual fear conditioning or exposure to a novel context. Using a novel CaMKII N beta-specific antibody, CaMKII N beta expression was analysed in the naïve mouse brain as well as in the amygdala and hippocampus after conditioning and context exposure. We show that in naïve mouse forebrain CaMKII N beta protein is expressed at its highest levels in olfactory bulb, prefrontal and piriform cortices, amygdala and thalamus. The protein is expressed both in dendrites and cell bodies. CaMKII N beta expression is rapidly and transiently up-regulated in the hippocampus after context exposure. In the amygdala, its expression is regulated only by contextual fear conditioning and not by exposure to a novel context. In conclusion, we show that CaMKII N beta expression is differentially regulated by novelty and contextual fear conditioning, providing further insight into molecular basis of fear LTM.
Publication status:
Published

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Publisher copy:
10.1111/j.1601-183x.2010.00595.x

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Journal:
Genes, brain, and behavior More from this journal
Volume:
9
Issue:
6
Pages:
648-657
Publication date:
2010-08-01
DOI:
EISSN:
1601-183X
ISSN:
1601-1848


Language:
English
Keywords:
Pubs id:
pubs:71213
UUID:
uuid:32f0f45b-dc80-44c7-b542-422517d85237
Local pid:
pubs:71213
Source identifiers:
71213
Deposit date:
2012-12-19

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