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Biol Psychiatry. 2005 Feb 15;57(4):433-6.

Transient N-methyl-D-aspartate receptor blockade in early development causes lasting cognitive deficits relevant to schizophrenia.

Author information

1
Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. stefani@bns.pitt.edu

Abstract

BACKGROUND:

Aberrant N-methyl-D-aspartate (NMDA) receptor-mediated glutamatergic transmission has been implicated in schizophrenia. We studied whether transient inhibition of NMDA receptor activity during early postnatal development would produce a behavioral phenotype resembling that of individuals who are susceptible to develop schizophrenia.

METHODS:

Rat pups were given injections of the NMDA channel blocker MK801 on postnatal days 7 through 10. This period is akin to the prenatal second trimester of primate development. Cognitive function was tested in adulthood.

RESULTS:

Treatment with MK801 impaired cognitive flexibility and working memory. The impairment in cognitive flexibility was due to increased perseverative behavior. Treatment did not affect locomotor activity or recognition memory.

CONCLUSIONS:

These results suggest that a brief disruption of NMDA receptors during a sensitive period of cortical development is sufficient to produce selective cognitive deficits that are relevant to schizophrenia.

PMID:
15705361
DOI:
10.1016/j.biopsych.2004.11.031
[Indexed for MEDLINE]
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