NMDAR Hypofunction Animal Models of Schizophrenia

被引：91

作者：

Lee, Gloria ^{[1
]}

Zhou, Yi ^{[1
]}

机构：

[1] Florida State Univ, Dept Biomed Sci, Coll Med, Tallahassee, FL 32306 USA

来源：

FRONTIERS IN MOLECULAR NEUROSCIENCE | 2019年 / 12卷

关键词：

NMDAR; NMDAR hypofunction; NMDAR antagonists; knockout mice; schizophrenia; animal models; 14-3-3; proteins; MEDIAL PREFRONTAL CORTEX; LONG-TERM POTENTIATION; D-ASPARTATE RECEPTORS; AUDITORY-EVOKED POTENTIALS; INDUCED COGNITIVE DEFICITS; TARGETED POINT MUTATIONS; SUBUNIT GENE GRIN2B; MICE LACKING; PREPULSE INHIBITION; 14-3-3; PROTEINS;

D O I：

10.3389/fnmol.2019.00185

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The N-methyl-d-aspartate receptor (NMDAR) hypofunction hypothesis has been proposed to help understand the etiology and pathophysiology of schizophrenia. This hypothesis was based on early observations that NMDAR antagonists could induce a full range of symptoms of schizophrenia in normal human subjects. Accumulating evidence in humans and animal studies points to NMDAR hypofunctionality as a convergence point for various symptoms of schizophrenia. Here we review animal models of NMDAR hypofunction generated by pharmacological and genetic approaches, and how they relate to the pathophysiology of schizophrenia. In addition, we discuss the limitations of animal models of NMDAR hypofunction and their potential utility for therapeutic applications.

引用

页数：26

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