Reversing behavioural abnormalities in mice exposed to maternal inflammation

Yeong Shin Yim, Ashley Park, Janet Berrios, Mathieu Lafourcade, Leila M. Pascual, Natalie Soares, Joo Yeon Kim, Sangdoo Kim, Hyunju Kim, Ari Waisman, Dan R. Littman, Ian R. Wickersham, Mark T. Harnett, Jun R. Huh () and Gloria B. Choi ()
Additional contact information
Yeong Shin Yim: McGovern Institute for Brain Research, Massachusetts Institute of Technology
Ashley Park: McGovern Institute for Brain Research, Massachusetts Institute of Technology
Janet Berrios: McGovern Institute for Brain Research, Massachusetts Institute of Technology
Mathieu Lafourcade: McGovern Institute for Brain Research, Massachusetts Institute of Technology
Leila M. Pascual: McGovern Institute for Brain Research, Massachusetts Institute of Technology
Natalie Soares: McGovern Institute for Brain Research, Massachusetts Institute of Technology
Joo Yeon Kim: McGovern Institute for Brain Research, Massachusetts Institute of Technology
Sangdoo Kim: University of Massachusetts Medical School
Hyunju Kim: University of Massachusetts Medical School
Ari Waisman: Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz
Dan R. Littman: Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine
Ian R. Wickersham: McGovern Institute for Brain Research, Massachusetts Institute of Technology
Mark T. Harnett: McGovern Institute for Brain Research, Massachusetts Institute of Technology
Jun R. Huh: University of Massachusetts Medical School
Gloria B. Choi: McGovern Institute for Brain Research, Massachusetts Institute of Technology

Nature, 2017, vol. 549, issue 7673, 482-487

Abstract: Abstract Viral infection during pregnancy is correlated with increased frequency of neurodevelopmental disorders, and this is studied in mice prenatally subjected to maternal immune activation (MIA). We previously showed that maternal T helper 17 cells promote the development of cortical and behavioural abnormalities in MIA-affected offspring. Here we show that cortical abnormalities are preferentially localized to a region encompassing the dysgranular zone of the primary somatosensory cortex (S1DZ). Moreover, activation of pyramidal neurons in this cortical region was sufficient to induce MIA-associated behavioural phenotypes in wild-type animals, whereas reduction in neural activity rescued the behavioural abnormalities in MIA-affected offspring. Sociability and repetitive behavioural phenotypes could be selectively modulated according to the efferent targets of S1DZ. Our work identifies a cortical region primarily, if not exclusively, centred on the S1DZ as the major node of a neural network that mediates behavioural abnormalities observed in offspring exposed to maternal inflammation.

Date: 2017
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DOI: 10.1038/nature23909

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