抄録
Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a ubiquitous serine/threonine protein kinase that is abundant in the brain as a major constituent of the postsynaptic density and critically involved in synaptic plasticity, learning and memory. Several behavioral abnormalities of CaMKIIα mutant mice were reported, but systematic assessments of CaMKIIα mutant mice have not been well conducted. To analyze the behavioral effects of CaMKIIα deficiency, we subjected CaMKIIα heterozygous knockout mice to a comprehensive behavioral test battery. The mutant mice showed increased locomotor activity, markedly decreased anxiety, decreased depression-related behavior, increased offensiveness, selective and severe spatial working memory deficit, and dramatic periodic change of locomotor activity in home cage. To identify the mechanism underlying the behavioral abnormalities of CaMKIIα mutant mice, gene expression analysis and biochemical analysis of the brain of the mutant mice were conducted. The potential involvement of CaMKIIα in pathogenesis/pathophysiology of psychiatric disorders, such as schizophrenia, bipolar disorder, and personality disorders, will be discussed. [J Physiol Sci. 2006;56 Suppl:S63]
