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Commentary| Volume 70, ISSUE 10, P906-907, November 15, 2011

Relating the Effects of Prenatal Stress in Rodents to the Pathogenesis of Schizophrenia

  • Holly Moore
    Correspondence
    Address correspondence to Holly Moore, Ph.D., Department of Psychiatry, Columbia University College of Physicians and Surgeons, New York, New York
    Affiliations
    Department of Psychiatry, Columbia University College of Physicians and Surgeons, New York, New York

    The New York State Psychiatric Institute, New York, New York
    Search for articles by this author
  • Ezra Susser
    Affiliations
    Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York

    The New York State Psychiatric Institute, New York, New York
    Search for articles by this author
      The study by Escobar et al. (
      • Escobar M.
      • Crouzin N.
      • Cavalier M.
      • Quentin J.
      • Roussel J.
      • Lanté F.
      • et al.
      Early, time-dependent disturbances of hippocampal synaptic transmission and plasticity after in utero immune challenge.
      ) in this issue shows that exposure of the pregnant rat dam at day 19 of gestation to a bacterial endotoxin, a manipulation used to model maternal immune activation (MIA), leads to abnormal postnatal development of synaptic long-term depression (LTD) in the CA3-CA1 hippocampal circuit in the offspring. The form of LTD they examined is induced by low-frequency stimulation of the glutamatergic efferents from CA3, which synapse extensively onto the dendrites of the CA1 projection neurons.
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