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Schizophr Res. 2016 Sep;176(1):72-82. doi: 10.1016/j.schres.2014.10.044. Epub 2014 Nov 20.

Behavioral sequelae of astrocyte dysfunction: focus on animal models of schizophrenia.

Author information

1
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, United States; Preclinical College, Guangxi University of Chinese Medicine, Nanning, 530001 Guangxi Province, China; Chinese Medicine College, Hubei University for Nationalities, ENSHI, 445000 Hubei Province, China.
2
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, United States.
3
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, United States; Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, United States; Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, United States; Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, United States. Electronic address: mpletnik@jhmi.edu.

Abstract

Astrocytes regulate multiple processes in the brain ranging from trophic support of developing neurons to modulation of synaptic neurotransmission and neuroinflammation in adulthood. It is, therefore, understandable that pathogenesis and pathophysiology of major psychiatric disorders involve astrocyte dysfunctions. Until recently, there has been the paucity of experimental approaches to studying the roles of astrocytes in behavioral disease. A new generation of in vivo models allows us to advance our understanding of the roles of astrocytes in psychiatric disorders. This review will evaluate the recent studies that focus on the contribution of astrocyte dysfunction to behavioral alterations pertinent to schizophrenia and will propose the possible solutions of the limitations of the existing approaches.

KEYWORDS:

Glutamate; Neuroinflammation; Neuron–astrocyte interaction; Psychiatric disorders; Tripartite synapse

PMID:
25468180
PMCID:
PMC4439390
DOI:
10.1016/j.schres.2014.10.044
[Indexed for MEDLINE]
Free PMC Article

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