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Combined effect of neonatal immune activation and mutant DISC1 on phenotypic changes in adulthood
Open accessAbstract
Gene-environment interaction may play a role in the etiology of schizophrenia. Transgenic mice expressing dominant-negative DISC1 (DN-DISC1 mice) show some histological and behavioral endophenotypes relevant to schizophrenia. Viral infection during neurodevelopment provides a major environmental risk for schizophrenia. Neonatal injection of polyriboinosinic-polyribocytidylic acid (polyI:C), which mimics innate immune responses elicited by viral infection, leads to schizophrenia-like behavioral alteration in mice after puberty. To study how gene-environmental interaction during neurodevelopment results in phenotypic changes in adulthood, we treated DN-DISC1 mice or wild-type littermates with injection of polyI:C during the neonatal stage, according to the published method, respectively, and the behavioral and histological phenotypes were examined in adulthood. We demonstrated that neonatal polyI:C treatment in DN-DISC1 mice resulted in the deficits of short-term, object recognition, and hippocampus-dependent fear memories after puberty, although polyI:C treatment by itself had smaller influences on wild-type mice. Furthermore, polyI:C-treated DN-DISC1 mice exhibited signs of impairment of social recognition and interaction, and augmented susceptibility to MK-801-induced hyperactivity as compared with vehicle-treated wild-type mice. Of most importance, additive effects of polyI:C and DN-DISC1 were observed by a marked decrease in parvalbumin-positive interneurons in the medial prefrontal cortex. These results suggest that combined effect of neonatal polyI:C treatment and DN-DISC1 affects some behavioral and histological phenotypes in adulthood.
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“Activated innate immune cells both produce and are activated by ROS: antioxidant therapy with NAC reduces the pathological and behavioural consequences of maternal LPS treatment and reduces foetal proinflammatory cytokine production 92,93 .”
From Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis (2016) · cites this paper as [93]
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Citations
Cites
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Background
Cited by
Sorted by citations
The environment and susceptibility to schizophrenia
Brown, A. S. (2011) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2010.09.003 · Cited by 664
Linking neurodevelopmental and synaptic theories of mental illness through DISC1
Brandon, N. J., & Sawa, A. (2011) · Nature reviews. Neuroscience · doi:10.1038/nrn3120 · Cited by 431
Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis
Hardingham, G. E., & Do, K. Q. (2016) · Nature Reviews Neuroscience · doi:10.1038/nrn.2015.19 · Cited by 304
Steullet, P., Cabungcal, J. H., Monin, A., Dwir, D., O'Donnell, P., Cuenod, M., & Do, K. Q. (2016) · Schizophrenia Research · doi:10.1016/j.schres.2014.06.021 · Cited by 262
“…combination has been demonstrated in transgenic mice expressing a putative dominant-negative disrupted in schizophrenia 1 (DN-DISC1), which display enhanced prefrontal oxidative stress (Johnson et al., 2013) and shows stronger PVI deficits following a postnatal immune challenge (Ibi et al., 2010).”
Prenatal interaction of mutant DISC1 and immune activation produces adult psychopathology
Abazyan, B., Nomura, J., Kannan, G., Ishizuka, K., Tamashiro, K. L., Nucifora, F., Pogorelov, V., Ladenheim, B., Yang, C., Krasnova, I. N., et al. (2010) · Biological Psychiatry · doi:10.1016/j.biopsych.2010.09.022 · Cited by 255
“In contrast to a previous study that injected Poly I:C into developing DISC1 mouse pups (36), we employed a widely used prenatal challenge with Poly I:C that is likely to be more relevant to the human situation, and to mimic maternal immune activation following microbial infections in humans (20–24).”
Metadata
- Authors
- Ibi, D., Nagai, T., Koike, H., Kitahara, Y., Mizoguchi, H., Niwa, M., Jaaro-Peled, H., Nitta, A., Yoneda, Y., & Nabeshima, T.
- Affiliations
- Nagoya University Hospital (JP)
- Nagoya University (JP)
- Kanazawa University (JP)
- Research Institute of Environmental Medicine, Nagoya University (JP)
- Johns Hopkins University (US)
- Meijo University (JP)
- ORCID
- Venue
- Behavioural Brain Research
- Publisher
- Elsevier BV
- Published
- 2010-01-05
- Volume
- 206
- Issue
- 1
- Pages
- 32-37
- ISSN
- 0166-4328 (ISSN-L)
- PMC
- PMC2846597
- OpenAlex
- W1988682809
- Cited by
- 137
- References
- 26
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 3 · 2023: 1 · 2022: 5 · 2021: 3 · 2020: 3 · 2019: 5 · 2018: 10 · 2017: 12 · 2016: 9 · 2015: 15 · 2014: 12 · 2013: 17 · 2012: 11
- FWCI
- 7.42
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Behavioural Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (P20MH084018, R01MH069853)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- schizophrenia, gene-environment interaction, DISC1, poly(I:C), viral infection, brain development, object recognition, social recognition, fear memory, hippocampus, parvalbumin interneurons, medial prefrontal cortex, transgenic mice
- MeSH terms
- Analysis of Variance, Animals, Animals, Newborn, Behavior, Animal, Conditioning, Classical, Fear, Female, Hippocampus, Hyperkinesis, Immunohistochemistry, Interferon Inducers, Male, Memory, Short-Term, Mice, Transgenic, Nerve Tissue Proteins, Parvalbumins, Phenotype, Poly I-C, Social Behavior, Staining and Labeling, Reflex, Startle, Dizocilpine Maleate, Ki-67 Antigen, Recognition, Psychology, Freezing Reaction, Cataleptic, Cell Proliferation, Mice, Sensory Gating
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