Abstract

CaMKII and long-term potentiation (LTP) were discovered within a decade of each other and have been inextricably intertwined ever since. However, like many marriages, it has had its up and downs. Based on the unique biochemical properties of CaMKII, it was proposed as a memory molecule before any direct physiological linkage was made to LTP. This review will assess the state of this marriage 40 years on. How well does the physiological evidence support the role of CaMKII in synaptic memory and what are the remaining outstanding issues?

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