Genetic animal models: focus on schizophrenia

被引:165
|
作者
Gainetdinov, RR [1 ]
Mohn, AR
Caron, MG
机构
[1] Duke Univ, Med Ctr, Howard Hughes Med Inst Labs, Dept Cell Biol, Durham, NC 27710 USA
[2] Duke Univ, Med Ctr, Howard Hughes Med Inst Labs, Dept Med, Durham, NC 27710 USA
关键词
D O I
10.1016/S0166-2236(00)01886-5
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The neurobiology of schizophrenia remains poorly understood. Symptoms of schizophrenia are classically thought to be associated with an imbalance of the dopaminergic system. However, the contribution of other neurotransmitters, in particular glutamate, has been increasingly appreciated. The role of individual components of neurotransmitter systems in aberrant behaviors can be experimentally tested in transgenic animals. Dopamine transporter knockout mice display persistently elevated dopaminergic tone and therefore might be appropriate substrates to evaluate the dopamine hypothesis. Similarly, NMDA receptor-deficient mice can be used to evaluate the glutamate hypothesis of schizophrenia. In this review we discuss how such animal models might be relevant for understanding the neurochemical underpinnings of certain manifestations of schizophrenia.
引用
收藏
页码:527 / 533
页数:7
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