Lack of barbering behavior in the phospholipase Cβ1 mutant mouse: A model animal for schizophrenia

Abstract

Summary Abnormal phospholipid metabolism has been implicated in the pathogenesis of schizophrenia, and phospholipase C (PLC) β1 was shown to be reduced in specific brain areas of patients with schizophrenia. However, the causal relationship of the PLCβ1 gene with the behavioral symptoms of schizophrenia remains unclear. Recent studies with the knockout (KO) mice for the PLCβ1 gene have revealed an array of interesting phenotypes, which along with other previous information makes the PLCβ1-KO mouse a good candidate for an animal model for schizophrenia. This also suggests that the PLCβ1-linked signaling pathways may be involved in the neural system whose function is disrupted in the pathogenesis of schizophrenia. In this chapter we will introduce various studies relevant to this issue, highlighting the social withdrawal phenotypes of the mutant, such as the lack of barbering behaviors. Introduction An animal model for a disease is expected to display endophenotypes, which are quantifiable phenotypes relevant to symptoms of the disease to be modeled (Braff and Freedman 2002; Gould and Gottesman 2006; van den Buuse et al. 2005). The endophenotypes currently pursued in schizophrenia models are: locomotive hyperactivity, sensorimotor gating deficit, deficits in social interaction, and cognitive deficits (e.g., learning and memory). Genetically modified mice targeted on candidate susceptibility genes have so far been generated as animal models for schizophrenia. ？ Cambridge University Press 2010.