Reversing behavioural abnormalities in mice exposed to maternal inflammation
Open accessAbstract
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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When focal cortical dysplasia is present, ASD-like behaviors occur; but when its development is prevented, ASD-like behaviors do not occur.
“When focal cortical dysplasia is present, ASD-like behaviors occur; but when its development is prevented, ASD-like behaviors do not occur [81].”
From The ASD Living Biology: from cell proliferation to clinical phenotype (2019) · cites this paper as [81]
MIA can also induce more complex cortical phenotypes such as focal cortical dysplasia, similar to those found in ASD.
“MIA can also induce more complex cortical phenotypes such as focal cortical dysplasia [81, 132], similar to those found in ASD [34] (Fig. 7).”
From The ASD Living Biology: from cell proliferation to clinical phenotype (2019) · cites this paper as [81]
The same fetal MIA perturbation of littermates causes patches of focal cortical dysplasia that have marked heterogeneity, analogous to heterogeneity found in cortex in unrelated individual ASD cases postmortem.
“The Choi and colleagues [132, 81] MIA ASD mouse model study showed that the same fetal MIA perturbation of littermates causes patches of focal cortical dysplasia that have marked heterogeneity, analogous to heterogeneity found in cortex in unrelated individual ASD cases postmortem [34] (Fig. 7).”
From The ASD Living Biology: from cell proliferation to clinical phenotype (2019) · cites this paper as [81]
Alterations of host immune responses by gut microbiota are closely linked to ASD-related symptoms.
“Alterations of the host immune responses by gut microbiota are closely linked to ASD-related symptoms.”
From Gut microbiota changes in children with autism spectrum disorder: a systematic review (2020) · cites this paper as [18]
Implicated cytokine pathways include IL-5, IL-15, IL-17, IL-17a, IL-10, IL-1b, TNF-α, TGF-β1 and IFNγ.
“The implicated cytokine pathways include, and not limited to, IL-5, IL-15, IL-17, IL-17a, IL-10, IL-1b, TNF-α, TGF-β1 and IFNγ [12, 18, 65, 66].”
From Gut microbiota changes in children with autism spectrum disorder: a systematic review (2020) · cites this paper as [18]
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References 47 · Cited by 303
- Authors
- Shin Yim, Y., Park, A., Berrios, J., Lafourcade, M., Pascual, L. M., Soares, N., Yeon Kim, J., Kim, S., Kim, H., Waisman, A., Littman, D. R., Wickersham, I. R., Harnett, M. T., Huh, J. R., & Choi, G. B.
- Affiliations
- McGovern Institute for Brain Research (US)
- University of Massachusetts Chan Medical School (US)
- University Medical Center of the Johannes Gutenberg University Mainz (DE)
- Howard Hughes Medical Institute (US)
- ORCID
- Venue
- Nature
- Published
- 2017-09-13
- Volume
- 549
- Issue
- 7673
- Pages
- 482-487
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC5796433
- OpenAlex
- W2754986416
- Cited by
- 303
- References
- 47
- Citations by year
- 2026: 20 · 2025: 27 · 2024: 25 · 2023: 30 · 2022: 45 · 2021: 45 · 2020: 36 · 2019: 32 · 2018: 33 · 2017: 9 · 2014: 1
- FWCI
- 10.00
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship@UMassChan (submittedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institute of Mental Health (R01MH106497, R01MH115037)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK110559, R01DK106351)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- maternal immune activation, prenatal viral infection, neurodevelopmental disorders, Th17 cells, primary somatosensory cortex, cortical abnormalities, sociability, repetitive behavior, artificial neural networks, behavioral phenotypes, mice
- MeSH terms
- Animals, Behavior, Animal, Mental Disorders, Female, Inflammation, Male, Mothers, Phenotype, Pregnancy, Pregnancy Complications, Infectious, Prenatal Exposure Delayed Effects, Social Behavior, Somatosensory Cortex, Pyramidal Cells, Mice, Th17 Cells
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