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Nonhuman primate model of schizophrenia using a noninvasive EEG method.

Ricardo Gil-da-Costa1, Gene R Stoner, Raynard Fung

  • 1Systems Neurobiology Laboratories, Salk Institute for Biological Studies, La Jolla, CA 92037.

Proceedings of the National Academy of Sciences of the United States of America
|August 21, 2013
PubMed
Summary

Researchers developed a nonhuman primate model for schizophrenia using ketamine. This model replicates sensory processing deficits observed in schizophrenia patients, offering new avenues for studying the disease and potential therapies.

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Area of Science:

  • Neuroscience
  • Psychiatry
  • Pharmacology

Background:

  • Schizophrenia is linked to impaired sensory processing and cognitive deficits.
  • Mismatch negativity (MMN) and P3a event-related potentials (ERPs) are reduced in schizophrenia and may serve as biomarkers.
  • NMDA receptor antagonists like ketamine induce schizophrenia-like symptoms and reduce MMN/P3a in humans.

Purpose of the Study:

  • To develop a nonhuman primate (NHP) model of schizophrenia using NMDA-receptor blockade.
  • To obtain neurophysiological measures comparable to human studies.
  • To investigate the effects of ketamine on sensory and cognitive function in NHPs.

Main Methods:

  • Developed methods for recording ERPs in humans and rhesus macaques.
  • Identified homologous MMN and P3a ERPs in both species using an auditory oddball paradigm.
Keywords:
brainmedicinemonkeyneurologypsychiatry

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  • Administered subanesthetic ketamine to NHPs to induce NMDA-receptor blockade.

    • Main Results:

    • Observed homologous MMN and P3a ERPs in humans and macaques.
    • Ketamine administration significantly decreased the amplitude of both MMN and P3a ERPs in macaques.
    • These findings mirror reductions seen in human schizophrenia patients and ketamine-challenged subjects.

    Conclusions:

    • A pharmacologically induced NHP model of schizophrenia using ketamine shows promise.
    • This model allows for EEG-guided investigations into cellular mechanisms and therapies for schizophrenia.
    • The model's relevance extends to other neuropsychiatric disorders linked to the glutamatergic system and ERP deficits.