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Data Acquisition and Analysis In Brainstem Evoked Response Audiometry In Mice
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Early auditory sensory processing deficits in mouse mutants with reduced NMDA receptor function.

Stephan Bickel1, Hans-Peter Lipp, Daniel Umbricht

  • 1Department of Neuroanatomy, Institute of Anatomy, University of Zurich, Zurich, Switzerland. stephan.bickel@anatom.unizh.ch

Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology
|August 23, 2007
PubMed
Summary

NR1 mutant mice exhibit sensory gating and startle habituation deficits relevant to schizophrenia. However, these mice did not fully replicate alterations in auditory evoked potentials (AEP) peak recovery function observed in patients.

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Area of Science:

  • Neuroscience
  • Psychiatry
  • Genetics

Background:

  • Schizophrenia is associated with cognitive deficits, particularly in sensory information processing.
  • These deficits manifest in paradigms like prepulse inhibition (PPI) and auditory evoked potentials (AEP).
  • NMDA receptor dysfunction is implicated in schizophrenia's sensory processing impairments.

Purpose of the Study:

  • To investigate the role of NMDA receptor signaling in sensory and sensorimotor gating deficits.
  • To model schizophrenia-related deficits using NR1 subunit hypomorphic mice.
  • To compare the performance of NR1 mutant mice and wild-type littermates across established paradigms.

Main Methods:

  • Utilized NR1 hypomorphic mice and wild-type littermates.
  • Assessed prepulse inhibition (PPI) and habituation of the auditory startle response.
  • Evaluated auditory evoked potentials (AEP) using paired tone and peak recovery paradigms.

Main Results:

  • NR1 mutant mice displayed impaired habituation and PPI of the auditory startle response.
  • Gating deficits in the paired tone paradigm were observed in NR1 mutants.
  • NR1 mutants showed altered AEP responses at short interstimulus intervals (ISIs) in the peak recovery paradigm, but not at long ISIs.

Conclusions:

  • NR1 hypomorphic mice successfully model sensory and sensorimotor gating deficits seen in schizophrenia.
  • These mice do not fully replicate the peak recovery function alterations observed in schizophrenia patients.
  • The study highlights the utility of NR1 mutant mice for investigating specific aspects of schizophrenia pathophysiology.