Research article summary (published 29 Sep 2009):

Increased expression of the NR2A NMDA receptor subunit in the prefrontal cortex of rats reared in isolation.

Full Abstract

A hypofunction of the N-methyl-D-aspartate (NMDA) receptor has been implicated in the pathophysiology of schizophrenia. Compelling evidence of altered NMDA receptor subunit expression in the schizophrenic brain has not, however, so far emerged. Rats reared in isolation exhibit several characteristics, including disturbed sensory gating, which resemble those seen in schizophrenia. To explore the possibility that NMDA receptor dysfunction may contribute to the behavioral and neurochemical consequences of rearing rats in isolation, we compared NMDA receptor subunit expression in brains of rats which were housed in isolation and which displayed a deficit in prepulse inhibition of the acoustic startle response with that of socially housed controls. An initial microarray analysis revealed a 1.26-fold increase in NR2A transcript in the prefrontal cortex, but not in the nucleus accumbens, of rats reared in isolation compared with those housed socially. In contrast, NR1, NR2B, NR2C, NR2D, NR3A, and NR3B subunit expression was unchanged in either brain area. In a second cohort of animals, in situ hybridization revealed increased NR2A mRNA expression in the medial prefrontal cortex, an observation that was substantiated by increased [(3)H]CGP39653 binding suggesting that NR2A receptor subunit protein expression was also elevated in the medial prefrontal cortex of the same animals. No changes in expression of NR1 or NR2B subunits were observed at both mRNA and protein level. Altered NR2A subunit expression in the medial prefrontal cortex of rats reared in isolation suggests that NMDA receptor dysfunction may contribute to the underlying pathophysiology of this preclinical model of aspects of schizophrenia. Copyright 2009 Wiley-Liss, Inc.

Author information

Author/s: Turnock-Jones, Julia J (JJ); Jennings, Carol A (CA); Robbins, Melanie J (MJ); Cluderay, Jane E (JE); Cilia, Jackie (J); Reid, Juliet L (JL); Taylor, Adam (A); Jones, Declan N C (DN); Emson, Piers C (PC); Southam, Eric (E);

Affiliation: Department of Neurobiology, Babraham Institute, Babraham, CB2 4AT, United Kingdom. julia.jones(-atsign-)cancer.org.uk

Journal and publication information

Publication Type: Journal Article

Journal: Synapse (New York, N.Y.) (Synapse), published in United States. (Language: eng)

Reference: 2009-Oct; vol 63 (issue 10) : pp 836-46

Dates: Created 2009/08/11; Completed 2009/10/26;

PMID: 19533626, status: MEDLINE (last retrieval date: 10/26/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

2-Amino-5-phosphonovalerate - analogs & derivatives; metabolism Acoustic Stimulation - adverse effects Animals Animals, Newborn Gene Expression Profiling - methods Gene Expression Regulation - physiology Indoles - metabolism Male Oligonucleotide Array Sequence Analysis - methods

Oligonucleotide Array Sequence Analysis - methods Prefrontal Cortex - metabolism Protein Binding - physiology Radioligand Assay - methods Rats Receptors, N-Methyl-D-Aspartate - genetics; metabolism Social Isolation Startle Reaction - physiology Tritium - metabolism

Associated Chemicals: Indoles (0) ; MDL 105519 (0) ; NR2A NMDA receptor (0) ; Receptors, N-Methyl-D-Aspartate (0) ; Tritium (10028-17-8) ; CGP 39653 (132472-31-2) ; 2-Amino-5-phosphonovalerate (76726-92-6)

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