NMDAR Hypofunction Animal Models of Schizophrenia

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 subj...

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Published inFrontiers in molecular neuroscience Vol. 12; p. 185
Main Authors Lee, Gloria, Zhou, Yi
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Research Foundation 31.07.2019
Frontiers Media S.A
Subjects
Animal models
Antagonists
Behavior
Dopamine
Etiology
Genes
Glutamic acid receptors
Human subjects
Kinases
knockout mice
Mental disorders
Metabolism
N-Methyl-D-aspartic acid receptors
Neuroscience
Neurosciences
NMDAR
NMDAR antagonists
NMDAR hypofunction
Psychiatry
Schizophrenia
Social interaction
Social research
Studies
Therapeutic applications
14-3-3 proteins
animal models
knockout mice
NMDAR antagonists
NMDAR
NMDAR hypofunction
schizophrenia
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Summary: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.
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Reviewed by: Dennis Kätzel, University of Ulm, Germany; Jae-Ick Kim, Ulsan National Institute of Science and Technology, South Korea
Edited by: Xiaona Du, Hebei Medical University, China
ISSN:1662-5099
1662-5099
DOI:10.3389/fnmol.2019.00185