Journal
NATURE
Volume 549, Issue 7673, Pages 482-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nature23909
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Funding
- Simons Foundation Autism Research Initiative
- Simons Foundation
- Hock E. Tan and K. Lisa Yang Center for Autism Research
- DFG [CRC/TRR 128, WA1600/8-1]
- Howard Hughes Medical Institute
- National Research Foundation of Korea [MEST-35B-2011-E00012, NRF-2014R1A1A1006089]
- Searle Scholars Program
- Pew Scholar for Biomedical Sciences
- Kenneth Rainin Foundation
- National Institutes of Health [R01DK106351, R01DK110559]
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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.
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