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Cited by 209Iron Metabolism and DisordersNeurogenesis and neuroplasticity mechanismsTrace Elements in Health

Perinatal iron deficiency alters apical dendritic growth in hippocampal CA1 pyramidal neurons

Jorgenson, Lyric A., Wobken, Jane D., Georgieff, Michael K.·2003·Developmental Neuroscience
DOI 10.1159/000075667
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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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  • In adulthood, long after iron repletion, long-term effects are observed in hippocampal structure and function, monoamine metabolism, and myelination.

    “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]

  • Prenatal inflammation can cause a cytokine-mediated reduction of circulating nonheme iron, or hypoferremia, which can disrupt fetal brain development and lead to persistent structural and functional brain defects.

    “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]

  • Prevention of iron deficiency might be key for protecting against adverse neurodevelopmental outcomes, and early developmental periods are critical.

    “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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Authors
Jorgenson, L. A., Wobken, J. D., & Georgieff, M. K.
Affiliations
University of Minnesota (US)
ORCID
Georgieff, Michael K.
Venue
Developmental Neuroscience
Publisher
S. Karger AG
Published
2003
Volume
25
Issue
6
Pages
412-420
ISSN
  • 0378-5866 (ISSN-L)
  • 1421-9859
DOI
10.1159/000075667
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
Licence
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

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