Pathogenic disruption of DISC1-serine racemase binding elicits schizophrenia-like behavior via D-serine depletion-Reference-Cited by-同舟云学术

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Pathogenic disruption of DISC1-serine racemase binding elicits schizophrenia-like behavior via D-serine depletion

Published:2012-07-17 Issue:5 Volume:18 Page:557-567
ISSN:1359-4184
Container-title:Molecular Psychiatry
language:en
Short-container-title:Mol Psychiatry

Author:

Ma T M,Abazyan S,Abazyan B,Nomura J,Yang C,Seshadri S,Sawa A,Snyder S H,Pletnikov M V

Publisher

Springer Science and Business Media LLC

Subject

Cellular and Molecular Neuroscience,Psychiatry and Mental health,Molecular Biology

Link

http://www.nature.com/articles/mp201297.pdf

Reference75 articles.

1. Goff DC, Coyle JT . The emerging role of glutamate in the pathophysiology and treatment of schizophrenia. Am J Psychiatry 2001; 158: 1367–1377.

2. Javitt DC, Zukin SR . Recent advances in the phencyclidine model of schizophrenia. Am J Psychiatry 1991; 148: 1301–1308.

3. Mothet JP, Parent AT, Wolosker H, Brady Jr RO, Linden DJ, Ferris CD et al. D-serine is an endogenous ligand for the glycine site of the N-methyl-D-aspartate receptor. Proc Natl Acad Sci U S A 2000; 97: 4926–4931.

4. Shleper M, Kartvelishvily E, Wolosker H . D-serine is the dominant endogenous coagonist for NMDA receptor neurotoxicity in organotypic hippocampal slices. 2005; 25: 9413–9417.

5. Panatier A, Theodosis DT, Mothet JP, Touquet B, Pollegioni L, Poulain DA et al. Glia-derived D-serine controls NMDA receptor activity and synaptic memory. Cell 2006; 125: 775–784.

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