ArticlePloS one2015
Lipopolysaccharide Exposure Induces Maternal Hypozincemia, and Prenatal Zinc Treatment Prevents Autistic-Like Behaviors and Disturbances in the Striatal Dopaminergic and mTOR Systems of Offspring.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 64 citations in OpenAlex.
- Prebiotic Treatment During Pregnancy Prevents Social Deficits Associated with Autism Spectrum Disorder-like Behavior Induced by Maternal Immune Activation.Microorganisms · 2025Article
- Zinc-nanoparticles alleviate the ovarian damage induced by bacterial lipopolysaccharide (LPS) in pregnant rats and their fetuses.Histochemistry and cell biology · 2023Article
- Paeoniflorin Attenuates Lipopolysaccharide-Induced Cognitive Dysfunction by Inhibition of Amyloidogenesis in Mice.International journal of molecular sciences · 2023Article
- Maternal Immune Activation Induced by Prenatal Lipopolysaccharide Exposure Leads to Long-Lasting Autistic-like Social, Cognitive and Immune Alterations in Male Wistar Rats.International journal of molecular sciences · 2023Article
- Immune activation during pregnancy exacerbates ASD-related alterations in Shank3-deficient mice.Molecular autism · 2023Article
- Metal Profiles in Autism Spectrum Disorders: A Crosstalk between Toxic and Essential Metals.International journal of molecular sciences · 2022Review
- Linking Puberty and the Gut Microbiome to the Pathogenesis of Neurodegenerative Disorders.Microorganisms · 2022Review
- S100B dysregulation during brain development affects synaptic SHANK protein networks via alteration of zinc homeostasis.Translational psychiatry · 2021Article
- Zinc Supplementation During Pregnancy Alleviates Lipopolysaccharide-Induced Glial Activation and Inflammatory Markers Expression in a Rat Model of Maternal Immune Activation.Biological trace element research · 2021Article
- Mice Born to Mothers with Gravida Traumatic Brain Injury Have Distorted Brain Circuitry and Altered Immune Responses.Journal of neurotrauma · 2021Article
- Virulence factor-related gut microbiota genes and immunoglobulin A levels as novel markers for machine learning-based classification of autism spectrum disorder.Computational and structural biotechnology journal · 2021Article
- Zinc.Advances in food and nutrition research · 2021Review
- The Metallome as a Link Between the "Omes" in Autism Spectrum Disorders.Frontiers in molecular neuroscience · 2021Review
- Maternal Immune Activation Induces Neuroinflammation and Cortical Synaptic Deficits in the Adolescent Rat Offspring.International journal of molecular sciences · 2020Article
- Bridging the species gap in translational research for neurodevelopmental disorders.Neurobiology of learning and memory · 2019Article
- LPS-induced sickness behavior is not affected by selenium but is switched off by psychogenic stress in rats.Veterinary research communications · 2019Article
- Pioglitazone abolishes cognition impairments as well as BDNF and neurotensin disturbances in a rat model of autism.Biology open · 2019Article
- A neurochemical hypothesis for the origin of hominids.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Article
- Autism phenotypes in ZnT3 null mice: Involvement of zinc dyshomeostasis, MMP-9 activation and BDNF upregulation.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism is characterized by social deficits, repetitive behaviors, and cognitive inflexibility. The risk factors appear to include genetic and environmental conditions, such as prenatal infections and maternal dietary factors. Previous investigations by our group have demonstrated that prenatal exposure to lipopolysaccharide (LPS), which mimics infection by gram-negative bacteria, induces autistic-like behaviors. To understand the causes of autistic-like behaviors, we evaluated maternal serum metal concentrations, which are involved in intrauterine development and infection/inflammation. We identified reduced maternal levels of zinc, magnesium, selenium and manganese after LPS exposure. Because LPS induced maternal hypozincemia, we treated dams with zinc in an attempt to prevent or ease the impairments in the offspring. We evaluated the social and cognitive autistic-like behaviors and brain tissues of the offspring to identify the central mechanism that triggers the development of autism. Prenatal LPS exposure impaired play behaviors and T-maze spontaneous alternations, i.e., it induced autistic-like behaviors. Prenatal LPS also decreased tyrosine hydroxylase levels and increased the levels of mammalian target of rapamycin (mTOR) in the striatum. Thus, striatal dopaminergic impairments may be related to autism. Moreover, excessive signaling through the mTOR pathway has been considered a biomarker of autism, corroborating our rat model of autism. Prenatal zinc treatment prevented these autistic-like behaviors and striatal dopaminergic and mTOR disturbances in the offspring induced by LPS exposure. The present findings revealed a possible relation between maternal hypozincemia during gestation and the onset of autism. Furthermore, prenatal zinc administration appears to have a beneficial effect on the prevention of autism.
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