Cited by 255Tryptophan and brain disordersSchizophrenia research and treatmentStress Responses and Cortisol

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Prenatal Interaction of Mutant DISC1 and Immune Activation Produces Adult Psychopathology

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Abazyan, Bagrat, Nomura, Jun, Kannan, Geetha, Ishizuka, Koko, Tamashiro, Kellie L., Nucifora, Frederick, Pogorelov, Vladimir, Ladenheim, Bruce, Yang, Chunxia, Krasnova, Irina N., Cadet, Jean Lud, Pardo, Carlos, Mori, Susumu, Kamiya, Atsushi, Vogel, Michael W., Sawa, Akira, Ross, Christopher A., Pletnikov, Mikhail V.·2010·Biological Psychiatry

DOI 10.1016/j.biopsych.2010.09.022PMC PMC3026608

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Abstract

Background Gene-environment interactions (GEI) are involved in the pathogenesis of mental diseases. We evaluated interaction between mutant human disrupted-in-schizophrenia 1 (mhDISC1) and maternal immune activation implicated in schizophrenia and mood disorders.Methods Pregnant mice were treated with saline or polyinosinic:polycytidylic acid at gestation day 9. Levels of inflammatory cytokines were measured in fetal and adult brains; expression of mhDISC1, endogenous DISC1, lissencephaly type 1, nuclear distribution protein nudE-like 1, glycoprotein 130, growth factor receptor-bound protein 2, and glycogen synthase kinase-3beta were assessed in cortical samples of newborn mice. Tissue content of monoamines, volumetric brain abnormalities, dendritic spine density in the hippocampus, and various domains of the mouse behavior repertoire were evaluated in adult male mice.Results Prenatal interaction produced anxiety, depression-like responses, and altered social behavior that were accompanied by decreased reactivity of the hypothalamic-pituitary-adrenal axis, attenuated serotonin neurotransmission in the hippocampus, reduced enlargement of lateral ventricles, decreased volumes of amygdala and periaqueductal gray matter and density of spines on dendrites of granule cells of the hippocampus. Prenatal interaction modulated secretion of inflammatory cytokines in fetal brains, levels of mhDISC1, endogenous mouse DISC1, and glycogen synthase kinase-3beta. The behavioral effects of GEI were observed only if mhDISC1 was expressed throughout the life span.Conclusions Prenatal immune activation interacted with mhDISC1 to produce the neurobehavioral phenotypes that were not seen in untreated mhDISC1 mice and that resemble aspects of major mental illnesses. Our DISC1 mouse model is a valuable system to study GEI relevant to mental illnesses.

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Authors: Abazyan, B., Nomura, J., Kannan, G., Ishizuka, K., Tamashiro, K. L., Nucifora, F., Pogorelov, V., Ladenheim, B., Yang, C., Krasnova, I. N., Cadet, J. L., Pardo, C., Mori, S., Kamiya, A., Vogel, M. W., Sawa, A., Ross, C. A., & Pletnikov, M. V.
Affiliations: University of Maryland, Baltimore (US)
Corresponding author: Pletnikov, Mikhail V.
ORCID: Nomura, Jun
Tamashiro, Kellie L.
Nucifora, Frederick
Ladenheim, Bruce
Yang, Chunxia
Cadet, Jean Lud
Pardo, Carlos
Mori, Susumu
Kamiya, Atsushi
Vogel, Michael W.
Sawa, Akira
Ross, Christopher A.
Pletnikov, Mikhail V.
Venue: Biological Psychiatry
Publisher: Elsevier BV
Published: 2010-12
Volume: 68
Issue: 12
Pages: 1172-1181
ISSN: 0006-3223 (ISSN-L)
DOI: 10.1016/j.biopsych.2010.09.022
PMC: PMC3026608
OpenAlex: W2068766837
Cited by: 255
References: 83
Citations by year: 2026: 2 · 2025: 6 · 2024: 11 · 2023: 9 · 2022: 15 · 2021: 11 · 2020: 11 · 2019: 15 · 2018: 18 · 2017: 13 · 2016: 24 · 2015: 24 · 2014: 16 · 2013: 24 · 2012: 32
FWCI: 9.07
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Biological Psychiatry (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute of Mental Health
Cell Science Research Foundation
National Institutes of Health
Topics: Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords: DISC1, gene-environment interaction, maternal immune activation, polyinosinic-polycytidylic acid, prenatal immune activation, schizophrenia, mood disorders, anxiety, depression-like behavior, social behavior, hypothalamic-pituitary-adrenal axis, serotonergic neurotransmission, lateral ventricle enlargement, amygdala, periaqueductal gray, glycogen synthase kinase-3β, inflammatory cytokines
MeSH terms: Glycogen Synthase Kinase 3 beta, Animals, Animals, Newborn, Atrophy, Behavior, Animal, Brain, Carrier Proteins, Corticosterone, Disease Models, Animal, Female, Male, Mice, Mutant Strains, Mice, Transgenic, Microtubule-Associated Proteins, Nerve Tissue Proteins, Poly I-C, Pregnancy, Prenatal Exposure Delayed Effects, Stress, Psychological, Biogenic Monoamines, Cytokines, Mood Disorders, Glycogen Synthase Kinase 3, 1-Alkyl-2-acetylglycerophosphocholine Esterase, Dendritic Spines, Cytokine Receptor gp130, Mice, GRB2 Adaptor Protein

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Prenatal Interaction of Mutant DISC1 and Immune Activation Produces Adult Psychopathology

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