The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.
Perinatal Iron Deficiency Alters Apical Dendritic Growth in Hippocampal CA1 Pyramidal Neurons
Abstract
Iron deficiency early in life is associated with cognitive disturbances that persist beyond the period of iron deficiency. Within cognitive processing circuitry, the hippocampus is particularly susceptible to insults during the perinatal period. During the hippocampal growth spurt, which is predominantly postnatal in rodents, iron transport proteins and their messenger RNA stabilizing proteins are upregulated, suggesting an increased demand for iron import during this developmental period. Rat pups deprived of iron during the perinatal period show a 30–40% decrease in hippocampal metabolic activity during postnatal hippocampal development. We hypothesized that this reduced hippocampal neuronal metabolism impedes developmental processes such as neurite outgrowth. The goals of the current study were to investigate the effects of perinatal iron deficiency on apical dendritic segment growth in the postnatal day (P) 15 hippocampus and to determine if structural abnormalities persist into adulthood (P65) following iron treatment. Qualitative and quantitative immunohistochemical analyses of dendritic structure and growth using microtubule-associated protein-2 as an index showed that iron-deficient P15 pups have truncated apical dendritic morphology in CA1 and a persistence of an immature apical dendritic pattern at P65. These results demonstrate that perinatal iron deficiency disrupts developmental processes in the hippocampal subarea CA1 and that these changes persist despite iron repletion. These structural abnormalities may contribute to the learning and memory deficits that occur during and following early iron deficiency.
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“Long-term effects are observed in adulthood, long after iron repletion, in hippocampal structure and function, monoamine metabolism, and myelination (55 -60), indicating that early developmental periods are critical and that prevention of iron de fi ciency might be key for protecting against adverse neurodevelopmental outcomes.”
From Maternal Intake of Supplemental Iron and Risk of Autism Spectrum Disorder (2014) · cites this paper as [60]
In the citing paper
“Prenatal in fl ammation can produce a cytokine-mediated reduction of circulating nonheme iron, or hypoferremia (48), that can disrupt fetal brain development and lead to persistent structural and functional brain defects (55 -60).”
From Maternal Intake of Supplemental Iron and Risk of Autism Spectrum Disorder (2014) · cites this paper as [60]
In the citing paper
“Long-term effects are observed in adulthood, long after iron repletion, in hippocampal structure and function, monoamine metabolism, and myelination (55 -60), indicating that early developmental periods are critical and that prevention of iron de fi ciency might be key for protecting against adverse neurodevelopmental outcomes.”
From Maternal Intake of Supplemental Iron and Risk of Autism Spectrum Disorder (2014) · cites this paper as [60]
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Metadata
- Authors
- Jorgenson, L. A., Wobken, J. D., & Georgieff, M. K.
- Affiliations
- University of Minnesota (US)
- Venue
- Developmental Neuroscience
- Publisher
- S. Karger AG
- Published
- 2003
- Volume
- 25
- Issue
- 6
- Pages
- 412-420
- ISSN
- 0378-5866 (ISSN-L)
- 1421-9859
- OpenAlex
- W2032730227
- Cited by
- 209
- References
- 52
- Citations by year
- 2026: 7 · 2025: 6 · 2024: 4 · 2023: 6 · 2022: 11 · 2021: 11 · 2020: 4 · 2019: 8 · 2018: 13 · 2017: 8 · 2016: 11 · 2015: 8 · 2014: 10 · 2013: 9 · 2012: 15
- FWCI
- 3.80
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Developmental Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD29421)
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Keywords
- hippocampal CA1, dendritic morphology, pyramidal neurons, iron repletion, MAP2, learning and memory impairment, iron transport proteins
- MeSH terms
- Iron Deficiencies, Animals, Animals, Newborn, Cell Differentiation, Dendrites, Female, Fluorescent Antibody Technique, Hippocampus, Iron, Male, Microtubule-Associated Proteins, Organ Size, Down-Regulation, Rats, Sprague-Dawley, Pyramidal Cells, Prenatal Nutritional Physiological Phenomena, Rats
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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