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      Maternal immune activation and strain specific interactions in the development of autism-like behaviors in mice

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          Abstract

          It is becoming increasingly apparent that the causes of autism spectrum disorders (ASD) are due to both genetic and environmental factors. Animal studies provide important translational models for elucidating specific genetic or environmental factors that contribute to ASD-related behavioral deficits. For example, mouse research has demonstrated a link between maternal immune activation and the expression of ASD-like behaviors. Although these studies have provided insights into the potential causes of ASD, they are limited in their ability to model the important interactions between genetic variability and environmental insults. This is of particular concern given the broad spectrum of severity observed in the human population, suggesting that subpopulations may be more susceptible to the adverse effects of particular environmental insults. It is hypothesized that the severity of effects of maternal immune activation on ASD-like phenotypes is influenced by the genetic background in mice. To test this, pregnant dams of two inbred strains (that is, C57BL/6J and BTBR T +tf/J) were exposed to the viral mimic polyinosinic-polycytidylic acid (polyI:C), and their offspring were tested for the presence and severity of ASD-like behaviors. To identify differences in immune system regulation, spleens were processed and measured for alterations in induced cytokine responses. Strain-treatment interactions were observed in social approach, ultrasonic vocalization, repetitive grooming and marble burying behaviors. Interestingly, persistent dysregulation of adaptive immune system function was only observed in BTBR mice. Data suggest that behavioral and immunological effects of maternal immune activation are strain-dependent in mice.

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          Author and article information

          Journal
          Transl Psychiatry
          Transl Psychiatry
          Translational Psychiatry
          Nature Publishing Group
          2158-3188
          March 2013
          12 March 2013
          1 March 2013
          : 3
          : 3
          : e240
          Affiliations
          [1 ]Department of Psychiatry and Behavioral Sciences, University of California , Davis, CA, USA
          [2 ]The M.I.N.D. Institute, University of California , Davis, CA, USA
          [3 ]Department of Medical Microbiology and Immunology, University of California , Davis, CA, USA
          [4 ]Department of Neurological Surgery, University of California, Davis. One Shields Avenue , Davis, CA, USA
          Author notes
          [* ]Psychiatry and Behavioral Sciences, M.I.N.D. Institute, University of California, Davis, One Shields Avenue , Davis, CA 95618, USA. E-mail: jschwartzer@ 123456ucdavis.edu
          Article
          tp201316
          10.1038/tp.2013.16
          3625915
          23481627
          130a5ee0-e5d9-4e7d-be51-72ff1222548c
          Copyright © 2013 Macmillan Publishers Limited

          This work is licensed under the Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/

          History
          : 29 November 2012
          : 12 January 2013
          : 14 January 2013
          Categories
          Original Article

          Clinical Psychology & Psychiatry
          polyi:c,maternal immune activation,btbr,autism spectrum disorders,mouse,gene-environment

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