Koh, H. -Y. Kim, D. Lee, J. Lee, S. Shin, H. -S. 2024-01-21T00:01:25Z 2024-01-21T00:01:25Z 2021-08-31 2008-02 1601-1848 https://pubs.kist.re.kr/handle/201004/133808 Abnormal phospholipid metabolism has been implicated in the pathogenesis of schizophrenia, and it was reported that phospholipase C (PLC) beta 1 is reduced in specific brain areas of patients with schizophrenia. However, the causal relationship of the PLC beta 1 gene with behavioral symptoms of schizophrenia remains unclear. To address this issue, we have examined the mutant mice lacking PLC beta 1 for schizophrenia-related phenotypes by performing various behavioral tests, including general locomotor activity, sensorimotor gating, social behaviors, and learning and memory. Phospholipase C beta 1 knockout mice showed hyperactivities in an open field. They showed impaired prepulse inhibition of acoustic startle response, which was ameliorated by a systemic administration of an antipsychotic D2-receptor antagonist, haloperidol. In addition, they showed abnormal social behaviors, such as lack of barbering behavior, socially recessive trait and lack of nesting behavior. Furthermore, they showed impaired performance in the delayed-non-match-to-sample T-maze test. The present results show that the PLC beta 1 mutant mice share some of the behavioral abnormalities that have been reported in patients with schizophrenia. Thus, the PLC beta 1-linked signaling pathways may be involved in the neural system whose function is disrupted in the pathogenesis of schizophrenia. English BLACKWELL PUBLISHING INDUCED DOPAMINE RELEASE PREPULSE INHIBITION ANIMAL-MODELS C ISOZYMES SCHIZOPHRENIA AMPHETAMINE RECEPTORS ABNORMALITIES TRANSMISSION DISORDER Deficits in social behavior and sensorimotor gating in mice lacking phospholipase C beta 1 Article 10.1111/j.1601-183X.2007.00351.x 1 GENES BRAIN AND BEHAVIOR, v.7, no.1, pp.120 - 128 GENES BRAIN AND BEHAVIOR 7 1 120 128 scie scopus 000252394100016 2-s2.0-38349025623 Behavioral Sciences Neurosciences Behavioral Sciences Neurosciences & Neurology Article INDUCED DOPAMINE RELEASE PREPULSE INHIBITION ANIMAL-MODELS C ISOZYMES SCHIZOPHRENIA AMPHETAMINE RECEPTORS ABNORMALITIES TRANSMISSION DISORDER haloperidol knockout mice locomotor hyperactivity phospholipase C beta 1 prepulse inhibition schizophrenia social behavior