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Meyer U, Nyffeler M, Schwendener S, Knuesel I, Yee BK, Feldon J. Relative prenatal and postnatal maternal contributions to schizophrenia-related neurochemical dysfunction after in utero immune challenge. Neuropsychopharmacology . 2008 Jan ; 33(2):441-56. PubMed Abstract

Comments on Paper and Primary News
Comment by:  Alan Brown
Submitted 11 May 2007 Posted 11 May 2007

The paper by Meyer and colleagues is of great interest and adds to a growing body of preclinical and epidemiologic literature implicating exposure to in utero infection as a risk factor for schizophrenia. One especially important feature of this paper is that poly I:C was administered during the equivalent of early to mid-gestation, the gestational period during which our group observed an association between serologically documented influenza exposure and risk of schizophrenia in an epidemiologic study. Furthermore, these investigators have examined both dopaminergic and glutamatergic effects of in utero infection. The differential effects of prenatal poly I:C on these two neurochemical systems during pre-and post-adolescence is intriguing. Hence, this work complements previous studies by several investigators in the field, including the Patterson, Zuckerman, and Fatemi labs, in demonstrating behavioral, pharmacologic, and neuropathological abnormalities analogous to those seen in schizophrenia following prenatal immune activation, and further supports the biological...  Read more

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Comment by:  Darryl Eyles
Submitted 18 May 2007 Posted 18 May 2007
  I recommend this paper

The prenatal infection model, whereby pregnant mice are exposed at various gestational times to a synthetic RNA (poly[I:C]) to induce immune activation stands as one of the best developmental animal models for schizophrenia. Firstly, the model is based in the epidemiology of the disease, with good evidence that maternal infection is a valid non-genetic risk factor for this disease. The model causes hyper-responsiveness to psychotomimetic agents, consistent with abnormal dopamine/glutamate signaling, as well as inducing deficits in sensory motor gating and attention. Many of these changes are reversed via the use of antipsychotic drugs. Therefore, this animal model is rare in that it possesses relatively good construct, face, and predictive validities.

In this study, Meyer’s group has varied the prenatal exposure window by making it much earlier—prenatal day (PND) 9—a time when there is perhaps less overt cellular differentiation in the brain compared to previous work where the exposure was at PND 15. Not only this, the authors go on to consider the effect of...  Read more

View all comments by Darryl Eyles
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