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GluN1 hypomorph mice exhibit wide-ranging behavioral alterations.

C Barkus1, L A Dawson, T Sharp

  • 1Department of Experimental Psychology, University of Oxford, Oxford OX1 3UD, UK. chris.barkus@psy.ox.ac.uk

Genes, Brain, and Behavior
|February 4, 2012
PubMed
Summary

GluN1(hypo) mice, a model for schizophrenia, show broad behavioral deficits, not specific to the disease. These global impairments question their utility as a selective schizophrenia model.

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Area of Science:

  • Neuroscience
  • Psychiatry
  • Behavioral Science

Background:

  • N-methyl-d-aspartate receptor (NMDA) antagonists like ketamine suggest reduced NMDA neurotransmission in schizophrenia.
  • GluN1 'hypomorph' (GluN1(hypo)) mice, with reduced NMDA receptor expression, are proposed as a schizophrenia model.

Purpose of the Study:

  • To evaluate the behavioral phenotype of GluN1(hypo) mice across various tests.
  • To determine if GluN1(hypo) mice serve as a specific model for schizophrenia.

Main Methods:

  • Administered a battery of behavioral tests to GluN1(hypo) mice.
  • Assessed naturalistic behaviors, anxiety, and cognitive functions (spatial and non-spatial memory).

Main Results:

  • GluN1(hypo) mice displayed impairments in all cognitive tests and reduced naturalistic behaviors (nesting, burrowing).

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  • Deficits were observed in both short- and long-term memory.
  • Anxiety test results were inconclusive, potentially confounded by hyperactivity.

    • Conclusions:

    • GluN1(hypo) mice exhibit widespread behavioral abnormalities, indicating a global impairment rather than a specific disease model.
    • The broad deficits challenge the utility of GluN1(hypo) mice as a selective model for schizophrenia.