PLC-β1 & Schizophrenia-related Behaviors
- PLC-β1 & Schizophrenia-related Behaviors
- phospholipase C-beta1; mice; schizophrenia
- Issue Date
Conference on PI-PLC Activity and Signaling
- Phospholipase β-1 (PLC-β1) is among the GPCR (G-protein-coupled receptor)-associated PLC-β isoforms that are known to be involved in many central nervous system (CNS) functions. PLC-β1 is expressed in select areas of brain such as cerebral cortex, hippocampus, amygdala, lateral septum, and olfactory bulb, and, therefore, is implicated for participations in diverse critical functions related to forebrain diseases such as schizophrenia. Abnormal phospholipid metabolism has been implicated in the pathogenesis of schizophrenia, and it was reported that PLC-β1 is reduced in specific brain areas of patients with schizophrenia. However, the causal relationship of the PLC-β1 gene with behavioral symptoms of schizophrenia remains unclear. To address this issue, we examined the mutant mice lacking PLC-β1 for schizophrenia-related phenotypes by performing various behavioral tests, including general locomotor activity, sensorimotor gating, social behaviors, and learning & memory. PLC-β1 knock-out mice showed hyperactivities in an open field. They showed impaired prepulse inhibition of acoustic startle response. In addition, they displayed abnormal social behaviors, such as, less preference for social novelty, lack of barbering behavior and nesting behavior. They also displayed working memory deficit shown by impaired performance in the delayed-non-match-to-sample (DNMTS) T-maze test. Some of these abnormalities were shown to be ameliorated by systemic administration of antipsychotics with various pharmacological profiles (e.g. haloperidol, aripiprazole, olanzapine, LY404039). The present results show that the PLC-β1 mutant mice share some of the behavioral abnormalities that have been reported in patients with schizophrenia. Thus, it is suggested that the some PLC-β1-linked signaling pathways are involved in the neural system whose function is disrupted in the pathogenesis of schizophrenia.
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