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Publication : Age-dependent changes in autophosphorylation of alpha calcium/calmodulin dependent kinase II in hippocampus and amygdala after contextual fear conditioning.

First Author  Fang T Year  2017
Journal  Brain Res Bull Volume  134
Pages  18-23 PubMed ID  28648815
Mgi Jnum  J:272166 Mgi Id  MGI:6282622
Doi  10.1016/j.brainresbull.2017.06.012 Citation  Fang T, et al. (2017) Age-dependent changes in autophosphorylation of alpha calcium/calmodulin dependent kinase II in hippocampus and amygdala after contextual fear conditioning. Brain Res Bull 134:18-23
abstractText  The hippocampus and amygdala are essential brain regions responsible for contextual fear conditioning (CFC). The autophosphorylation of alpha calcium-calmodulin kinase II (alphaCaMKII) at threonine-286 (T286) is a critical step implicated in long-term potentiation (LTP), learning and memory. However, the changes in alphaCaMKII levels with aging and training in associated brain regions are not fully understood. Here, we studied how aging and training affect the levels of phosphorylated (T286) and proportion of phosphorylated:total alphaCaMKII in the hippocampus and amygdala. Young and aged mice, naive (untrained) and trained in CFC, were analysed by immunohistochemistry for the levels of total and phosphorylated alphaCaMKII in the hippocampus and amygdala. We found that two hours after CFC training, young mice exhibited a higher level of phosphorylated and increased ratio of phosphorylated:total alphaCaMKII in hippocampal CA3 stratum radiatum. Furthermore, aged untrained mice showed a higher ratio of phosphorylated:total alphaCaMKII in the CA3 region of the hippocampus when compared to the young untrained group. No effect of training or aging were seen in the central, lateral and basolateral amygdala regions, for both phosphorylated and ratio of phosphorylated:total alphaCaMKII. These results show that aging impairs the training-induced upregulation of autophosphorylated (T286) alphaCaMKII in the CA3 stratum radiatum of the hippocampus. This indicates that distinct age-related mechanisms underlie CFC that may rely more heavily on NMDA receptor-dependent plasticity in young age.
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