The behavioral characterization reveals discrete effects of the KO, providing a foundation for future investigations. For example, this is the first description of a cre/loxP system for modulation of CaMKIIb knockout, thereby allowing a more precise analysis of CaMKIIb function specific cell types, Avastin tissues or Trimetazidine dihydrochloride development stages in future research. The results presented here are in agreement with data from an independently generated CaMKIIb KO mouse, in that our CaMKIIb KO mouse also shows a lack of motor coordination, and exhibits cognitive impairments. In addition, we show here that CaMKIIb KO mice have decreased levels of anxiety-related behavior and a developmental delay in body weight gain. This study extends previous work on the CaMKIIb isoform, clearly demonstrating the fundamental importance of CaMKIIb isoform in many aspects of the mouse behavior. Global deletion of CaMKIIb resulted in ataxia, which largely affected forelimb coordination and strength, as observed by watching the movement of the mice, and measured experimentally by the grip strength analysis. Body mass composition indicates that this effect was not due to less muscle mass; therefore, the grip strength deficit appears to be nervous system dependent. Interestingly, the motor impairments required a total loss of the CaMKIIb, as the CaMKIIb+/2 mice were found to have no motor impairments. CaMKIIb is known to have critical roles in cerebellar Purkinje cell synaptic function ; thus, it would be logical to assume that the ataxia is cerebellar in origin. In addition to the high expression of CaMKIIb in the cerebellum, our results also demonstrate high levels of CaMKIIb in the basal ganglia circuit, in agreement with previous studies showing CaMKIIb expression in tyrosine hydroxylase positive neurons in the substantia nigra and in striatal medium spiny neurons. CaMKIIb has also been reported to have important functions in oligodendrocyte maturation and in myelination. Therefore, motor impairments in our CaMKIIb KO mice could be a result of myelin deficits in the spinal cord, basal ganglia dysfunction, or cerebellar dysfunction.