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Mice with subtle reduction of NMDA NR1 receptor subunit expression have a selective decrease in mismatch negativity:

Robert E Featherstone1, Rick Shin2, Jeffrey H Kogan2

  • 1Translational Neuroscience Program, Department of Psychiatry, University of Pennsylvania, Philadelphia, PA, USA.

Neurobiology of Disease
|December 3, 2014
PubMed
Summary
This summary is machine-generated.

Heterozygous NR1 knockdown mice exhibit reduced auditory mismatch negativity, offering a sensitive model for studying schizophrenia's glutamate dysfunction. These findings align with human studies, suggesting a potential for novel therapeutic targets.

Keywords:
EEGMismatch negativityMouseNMDASchizophrenia

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Area of Science:

  • Neuroscience
  • Psychiatry
  • Genetics

Background:

  • Glutamate dysfunction is implicated in schizophrenia pathogenesis.
  • Existing animal models for studying glutamate deficits in schizophrenia have limitations, including transient effects or overly severe phenotypes.
  • There is a need for sensitive models that reflect developmental and sustained reductions in glutamate function.

Purpose of the Study:

  • To investigate schizophrenia-related electroencephalogram (EEG) measures in mice with heterozygous NR1 subunit gene alteration (NR1+/-).
  • To assess the utility of NR1+/- mice as a model for studying subtle changes in glutamate function relevant to schizophrenia.

Main Methods:

  • Utilized NR1+/- mice with a 30% reduction in NR1 receptor expression.
  • Assessed EEG measures including auditory event-related potentials (ERPs), gamma power, and mismatch negativity (MMN) in response to auditory stimuli.
  • Compared NR1+/- mice to homozygous NR1-/- mice and NMDA antagonist models.

Main Results:

  • NR1+/- mice showed no significant changes in obligatory ERPs (P20, N40) or baseline/evoked gamma power.
  • NR1+/- mice exhibited a marked reduction in mismatch negativity (MMN) response to deviant auditory tones.
  • These deficits in NR1+/- mice were distinct from the transient effects of NMDA antagonists and the more severe phenotypes of NR1-/- mice.

Conclusions:

  • EEG response to deviant auditory stimuli, specifically MMN, is a sensitive indicator of subtle glutamate function deficits.
  • NR1+/- mice represent a promising and sensitive animal model for studying schizophrenia vulnerability and glutamate dysfunction.
  • The findings in NR1+/- mice align with human studies showing MMN deficits in schizophrenia patients and their families.