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Animal Models

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Animal Model: Grin1D481N NR1 Point Mutation
Preparation Type: Genetic Preparations
Gating: Persistent latent inhibition; no PPI deficit; increased startle reactivity
Cognitive behavior: Spatial recognition impairments
Social behavior: Social approach deficits
Molecular/morphological signature: Reduced NMDAR glycine affinity; reduced LTP in hippocampus
Response to APD: Phenotype reversed by D-serine treatment as well as D-amino acid oxidase gene deletion
Citations: Labrie V, Lipina T, Roder JC. Mice with reduced NMDA receptor glycine affinity model some of the negative and cognitive symptoms of schizophrenia. Psychopharmacology (Berl). 2008 Oct 1; 200(2):217-30. Abstract

Labrie V, Clapcote SJ, Roder JC. Mutant mice with reduced NMDA-NR1 glycine affinity or lack of D-amino acid oxidase function exhibit altered anxiety-like behaviors. Pharmacol Biochem Behav. 2009 Feb;91(4):610-20. Abstract

Duffy S, Labrie V, Roder JC. D-serine augments NMDA-NR2B receptor-dependent hippocampal long-term depression and spatial reversal learning. Neuropsychopharmacology. 2008 Apr;33(5):1004-18. Abstract

Kew JN, Koester A, Moreau JL, Jenck F, Ouagazzal AM, Mutel V, Richards JG, Trube G, Fischer G, Montkowski A, Hundt W, Reinscheid RK, Pauly-Evers M, Kemp JA, Bluethmann H. Functional consequences of reduction in NMDA receptor glycine affinity in mice carrying targeted point mutations in the glycine binding site. J Neurosci. 2000 Jun 1;20(11):4037-49. Abstract

Ballard TM, Pauly-Evers M, Higgins GA, Ouagazzal AM, Mutel V, Borroni E, Kemp JA, Bluethmann H, Kew JN. Severe impairment of NMDA receptor function in mice carrying targeted point mutations in the glycine binding site results in drug-resistant nonhabituating hyperactivity. J Neurosci. 2002 Aug 1;22(15):6713-23. Abstract


December 20, 2014
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