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

作者：Radwanska K; Tudor Jones A A; Mizuno K; Pereira G S; Lucchesi W; Alfano I; Lach A; Kaczmarek L; Knapp S; Giese K Peter^*

来源：Genes, Brain and Behavior, 2010, 9(6): 648-657.

DOI：10.1111/j.1601-183X.2010.00595.x

• alpha CaMKII
• amygdala
• CaMKII N beta
• context
• fear memory
• hippocampus

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 naive mouse brain as well as in the amygdala and hippocampus after conditioning and context exposure. We show that in naive mouse forebrain CaMKII 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.

• 出版日期2010-8