Ca²⁺/calmodulin-dependent protein kinase IIα (CaMKIIα) is one of the most abundant protein kinases in the central nervous system, and is thought to be a key mediator for hippocampal synaptic plasticity. We previously reported differential involvement of kinase activity of CaMKIIα in hippocampus- vs. amygdala-dependent memory by behavioral analysis of fear conditioning in the kinase-dead CaMKIIα knock-in (CaMKIIα-KI) mouse: Hippocampus-dependent memory was severely impaired, whereas amygdala-dependent memory was only partially impaired. To elucidate more in detail about which types of memory are under control of CaMKIIα, here we performed Morris water maze tasks using the CaMKIIα-KI mouse. In visible platform trials, both CaMKIIα-KI and wild-type (WT) mice could learn to reach the platform in a similar way. On the other hand, in hidden platform trials, WT mice could still reach the platform, but CaMKIIα-KI mice could not. The probe trial revealed that WT mice selectively searched the target quadrant, whereas CaMKIIα-KI mice randomly searched the four quadrants. These results indicate that visually guided memory acquisition is intact, while spatial memory acquisition is severely impaired in the kinase-dead CaMKIIα-KI mouse, supporting the selectivity of its memory deficits in the hippocampus. We are currently performing another type of memory acquisition task, i.e., cross maze task to examine whether striatum-dependent memory acquisition is intact or not. With all these data, we will discuss which types of memory are truly under control of kinase activity of CaMKIIα.