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Learning and memory is widely believed to result from changes in connectivity within neuronal circuits due to synaptic plasticity. Work over the past two decades has shown that Ca(2+) influx during LTP induction triggers the activation of CaMKII in dendritic spines. CaMKII activation results in autophosphorylation of the kinase rendering it constitutively active long after the Ca(2+) dissipates within the spine. This "molecular switch"(1) mechanism is essential for LTP and learning and memory. Here, we discuss this key regulatory mechanism and the diversity of downstream targets that can be modulated by CaMKII to exert dynamic control of synaptic structure and function.
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