The cerebellum is in charge of the smooth coordination of somatic motor activity, regulation of muscle tone, and mechanisms that influence and maintain equilibrium [30]. It is widely accepted that the cerebellum is involved in the performance of the rotating rod task, since mice with structural abnormalities in the cerebellum [31] or with disruptions in genes enriched in the cerebellum [32] exhibit performance deficits in this task. In the rotating rod test in this study, although the retention time of ADAM11-deficient mice on the rod was not different from wild-type mice at 0 rpm (stationary), ADAM11-deficient mice fell more quickly from the rod than wild-type mice at 5, 10 and 15 rpm. These results indicate that ADAM11-deficient mice have a deficit in motor coordination. On the other hand, in the visual platform version of the water maze task, motor ability for swimming in ADAM11-deficient mice was normal. These results suggested that there might be a different mechanism of motor function between swimming and the rotating rod task. It has been also reported that the cerebellum is involved in another important distinct function: learning associated with component movement (motor learning) [33]. The retention time of synaptotagmin (Syt) IV-deficient mice on the rod was significantly shorter than wild-type mice, and they improved it approximately to the same rates as did wild-type mice during rotating rod performance [34]. These data suggest the basis for the performance deficit on the rotating rod task in the Syt IV mutants is in motor coordination rather than in motor learning. The results in the present study showed that ADAM11-deficient mice slightly, though not significantly, improved motor learning ability during rotating rod performance. However, the deficit of motor learning in ADAM11-deficient mice was not clear in this study. Because they could not ride on the rotating rod, they might not learn this task. To examine motor learning ability in ADAM11-deficient mice in detail, we will need to use other cerebellar-dependent learning tasks, such as a classical eyelid conditioning test. There was no impairment in the grip strength and wire suspension test in ADAM11-deficient mice. Spontaneous motor activity and walking patterns of ADAM11-deficient mice were also found to be normal, suggesting that the dysfunction found in the rotating rod test was not derived from muscle weakness or other peripheral disturbances.