Institute of Biochemistry and Cell Biology, University of Magdeburg, Leipziger Straße 44, 39120 Magdeburg, Germany.
Neural Plast. 2012;2012:832757. doi: 10.1155/2012/832757. Epub 2012 Oct 24.
Schizophrenia is a complex psychiatric disorder. Although a number of different hypotheses have been developed to explain its aetiopathogenesis, we are far from understanding it. There is clinical and experimental evidence indicating that neurodevelopmental factors play a major role. Disturbances in neurodevelopment might result in alterations of neuroanatomy and neurochemistry, leading to the typical symptoms observed in schizophrenia. The present paper will critically address the neurodevelopmental models underlying schizophrenia by discussing the effects of typical and atypical antipsychotics in animal models. We will specifically discuss the vitamin D deficiency model, the poly I:C model, the ketamine model, and the postnatal ventral hippocampal lesion model, all of which reflect core neurodevelopmental issues underlying schizophrenia onset.
精神分裂症是一种复杂的精神疾病。尽管已经提出了许多不同的假说来解释其病因发病机制,但我们远未完全理解它。有临床和实验证据表明,神经发育因素起着重要作用。神经发育障碍可能导致神经解剖和神经化学的改变,从而导致精神分裂症的典型症状。本文将通过讨论典型和非典型抗精神病药物在动物模型中的作用,批判性地探讨精神分裂症的神经发育模型。我们将特别讨论维生素 D 缺乏模型、聚 I:C 模型、氯胺酮模型和产后海马腹侧损伤模型,这些模型都反映了精神分裂症发病的核心神经发育问题。