Activation of alpha-CaM KII During Mammalian Associative Learning

Autophosphorylation of calcium/calmodulin-dependent protein kinase II (CaM KII) converts it to an autonomously active form, which remains persistently active even in the absence of calcium. Recently, autophosphorylation of CaM KII has been found to be required for hippocampal long-term potentiation (LTP), a form of synaptic plasticity that is a potential cellular mechanism of learning and memory. These findings led us to hypothesize that autophosphorylation of CaM KII increases during learning and memory. To test this hypothesis, animals were trained to associate a foot shock with a context and cue, then homogenates of various brain regions were assayed for changes in CaM KII autophosphorylation. Using a specific antibody that detects autophosphorylated CaM KII, Promega’s Anti-ACTIVE^® CaM KII pAb (Cat.# V1111), we observed an increase in immunoreactivity in the hippocampus of trained animals in comparison to naive animals. It appears that CaM KII is autophosphorylated in the hippocampus as a result of classical conditioning in mammals.

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