The Academic Frontier Project for Private University, Comparative Cognitive Science Institute, Meijo University, Japan.
Biol Pharm Bull. 2011;34(9):1358-63. doi: 10.1248/bpb.34.1358.
Accumulating evidence supports the existence of an overlap in genetic susceptibility with schizophrenia. Translation of human genetic mutations into animals is one of the most important strategies to study the pathogenesis of schizophrenia, identify potential drug targets, and test new medicines for antipsychotic treatment. Recent discoveries of susceptibility genes for schizophrenia make the possibility to develop newer genetic mouse models based on the neurodevelopmental hypotheses of schizophrenia. Although it is not possible to mimic all schizophrenic symptoms by these animal models, the genetic mouse models based on the neurodevelopmental hypothesis are widely developed to reproduce several schizophrenia-like behavioral and biochemical changes in humans. In this mini review, we will discuss the neuropathological and behavioral manifestations of representative genetic mouse models for schizophrenia, associated with the hypothesis of abnormal neurodevelopment.
越来越多的证据支持精神分裂症与遗传易感性重叠的存在。将人类基因突变转化为动物模型是研究精神分裂症发病机制、确定潜在药物靶点和测试新型抗精神病治疗药物的最重要策略之一。最近发现的精神分裂症易感基因使得基于精神分裂症神经发育假说开发新型遗传小鼠模型成为可能。尽管这些动物模型不可能模拟所有的精神分裂症症状，但基于神经发育假说的遗传小鼠模型被广泛开发，以在人类中再现几种类似精神分裂症的行为和生化变化。在这篇综述中，我们将讨论与神经发育异常假说相关的、具有代表性的精神分裂症遗传小鼠模型的神经病理学和行为表现。
