The DOI matches its Crossref record; 77 of the 77 references it cites were found in a registry or an index.
Neurodevelopmental damage after prenatal infection: Role of oxidative stress in the fetal brain
Abstract
Prenatal infection is a major risk responsible for the occurrence of psychiatric conditions in infants. Mimicking maternal infection by exposing pregnant rodents to bacterial endotoxin lipopolysaccharide (LPS) also leads to major brain disorders in the offspring. The mechanisms of LPS action remain, however, unknown. Here, we show that LPS injection during pregnancy in rats, 2 days before delivery, triggered an oxidative stress in the hippocampus of male fetuses, evidenced by a rapid rise in protein carbonylation and by decreases in alpha-tocopherol levels and in the ratio of reduced/oxidized forms of glutathione (GSH/GSSG). Neither protein carbonylation increase nor decreases in alpha-tocopherol levels and GSH/GSSG ratio were observed in female fetuses. NMDA synaptic currents and long-term potentiation in CA1, as well as spatial recognition in the water maze, were also impaired in male but not in female 28-day-old offspring. Pretreatment with the antioxidant N-acetylcysteine prevented the LPS-induced changes in the biochemical markers of oxidative stress in male fetuses, and the delayed detrimental effects in male 28-day-old offspring, completely restoring both long-term potentiation in the hippocampus and spatial recognition performance. Oxidative stress in the hippocampus of male fetuses may thus participate in the neurodevelopmental damage induced by a prenatal LPS challenge.
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“Such augmented disruption occurs via the activation of the cellular redox signaling in response to infection [130,133].”
From The ASD Living Biology: from cell proliferation to clinical phenotype (2019) · cites this paper as [133]
In the citing paper
“This deleterious effect could result from a redox dysregulation as maternal immune challenge transiently decreases GSH and vitamin E levels and increase oxidative stress in the hippocampus (Lante et al., 2007).”
From Redox dysregulation, neuroinflammation, and NMDA receptor hypofunction: A “central hub” in schizophrenia pathophysiology? (2016) · cites this paper as Lante et al., 2007
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“Indeed, severe immobilization stress to pregnant rats produced deficits in spatial learning [67] and in LTP [68] in the offspring, together with a remodeling of NMDA receptors, with a relative decrease in the NR2B and increase in the NR2A subunits.”
BackgroundNMDA receptor hypofunction model of schizophrenia
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Berk, M., Kapczinski, F., Andreazza, A. C., Dean, O. M., Giorlando, F., Maes, M., Yücel, M., Gama, C. S., Dodd, S., Dean, B., et al. (2011) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2010.10.001 · Cited by 1,178
The role of inflammation in perinatal brain injury
Hagberg, H., Mallard, C. E., Ferriero, D. M., Vannucci, S. J., Levison, S. W., Vexler, Z. S., & Gressèns, P. (2015) · Nature Reviews Neurology · doi:10.1038/nrneurol.2015.13 · Cited by 852
Neuromodulatory properties of inflammatory cytokines and their impact on neuronal excitability
Vezzani, A., & Viviani, B. (2015) · Neuropharmacology · doi:10.1016/j.neuropharm.2014.10.027 · Cited by 670
Boksa, P. (2010) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2010.03.005 · Cited by 603
Oxidative stress in schizophrenia: An integrated approach
Bitanihirwe, B. K. Y., & Woo, T.-U. W. (2010) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2010.10.008 · Cited by 482
Metadata
- Authors
- Lanté, F., Meunier, J., Guiramand, J., Maurice, T., Cavalier, M., de Jesus Ferreira, M.-C., Aimar, R., Cohen-Solal, C., Vignes, M., & Barbanel, G.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Barbanel, Gérard
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2007-04
- Volume
- 42
- Issue
- 8
- Pages
- 1231-1245
- ISSN
- 0891-5849 (ISSN-L)
- OpenAlex
- W1987843838
- Cited by
- 140
- References
- 77
- Citations by year
- 2026: 5 · 2025: 2 · 2024: 6 · 2023: 7 · 2022: 4 · 2021: 6 · 2020: 5 · 2019: 6 · 2018: 7 · 2017: 7 · 2016: 12 · 2015: 16 · 2014: 10 · 2013: 9 · 2012: 14
- FWCI
- 5.36
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
- Life Sciences › Neuroscience › Developmental Neuroscience › Anesthesia and Neurotoxicity Research
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- prenatal infection, lipopolysaccharide, oxidative stress, fetal hippocampus, neurodevelopmental damage, protein carbonylation, alpha-tocopherol, glutathione, long-term potentiation, spatial recognition, sex differences, N-acetylcysteine, maternal infection, rodent models
- MeSH terms
- Animals, Brain, Brain Diseases, Chromatography, High Pressure Liquid, Female, Glutathione, Hippocampus, Infections, Lipopolysaccharides, Pregnancy, Rats, Sprague-Dawley, Oxidative Stress, Patch-Clamp Techniques, Glutathione Disulfide, alpha-Tocopherol, Rats
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