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Cited by 162Iron Metabolism and DisordersNeuroscience and Neuropharmacology ResearchTrace Elements in Health

Fetal iron deficiency disrupts the maturation of synaptic function and efficacy in area CA1 of the developing rat hippocampus

Jorgenson, Lyric A., Sun, Mu, O'Connor, Michael, Georgieff, Michael K.·2005·Hippocampus
DOI 10.1002/hipo.20128
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Abstract

Late fetal and early postnatal iron deficiency (ID) is a common condition that causes learning and memory impairments in humans while they are iron deficient and following iron repletion. Rodent models of fetal ID demonstrate significant short- and long-term hippocampal structural and biochemical abnormalities that may predispose hippocampal area CA1 to abnormal electrophysiology. Rat pups made iron deficient during the fetal and early postnatal period were assessed for basal synaptic transmission, paired-pulse facilitation (PPF), and long-term potentiation (LTP) in CA1 at postnatal days (P)15 and P30 while iron deficient and at P65 following iron repletion. Our results showed no differences in basal synaptic transmission between iron sufficient and iron deficient pups at P15 or P30, but the ID group did fail to demonstrate the expected developmental increase in synaptic strength by P65 (P < 0.05). Similarly, PPF ratios from iron deficient slices also failed to demonstrate the characteristic developmental changes seen in the iron sufficient group (P < 0.001). Iron deficient slices retained a developmentally immature P15 pattern of LTP expression at P30 and after iron repletion, and LTP expression was lower (P < 0.05) in the iron deficient group at P65. Thus, ID in the fetal and early postnatal period delays or abolishes the developmental maturation of electrophysiological components of synaptic efficacy and plasticity, resulting in abnormalities beyond the period of deficiency. These findings provide a functional corroboration to previous structural and biochemical abnormalities found in the iron deficient rat hippocampus and provide a potential model for learning and memory deficits seen in humans exposed to fetal and early postnatal ID.

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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 [59]

  • 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 [59]

  • 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 [59]

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Authors
Jorgenson, L. A., Sun, M., O'Connor, M., & Georgieff, M. K.
Affiliations
University of Minnesota (US)
Corresponding author
Georgieff, Michael K.
ORCID
Venue
Hippocampus
Publisher
Wiley
Published
2005
Volume
15
Issue
8
Pages
1094-1102
ISSN
  • 1050-9631 (ISSN-L)
  • 1098-1063
DOI
10.1002/hipo.20128
OpenAlex
W1991297975
Cited by
162
References
62
Citations by year
2026: 1 · 2025: 6 · 2024: 4 · 2023: 8 · 2022: 5 · 2021: 6 · 2020: 6 · 2019: 6 · 2018: 6 · 2017: 7 · 2016: 8 · 2015: 8 · 2014: 13 · 2013: 12 · 2012: 14
FWCI
4.53
Type
journal article
Language
en
Open access
closed
Licence
doi.wiley.com/10.1002/tdm_license_1.1 (tdm, 3895 d)
Locations
  • Hippocampus (publishedVersion)
  • PubMed (publishedVersion)
Funders
Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD29421)
Topics
  • Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
Keywords
synapse maturation, synaptic transmission, paired-pulse facilitation, long-term potentiation, synaptic plasticity, iron repletion, learning and memory impairment, rat model
MeSH terms
Iron Deficiencies, Animals, Disease Models, Animal, Fetal Diseases, Hippocampus, Iron, Learning, Male, Memory, Synaptic Transmission, Neuronal Plasticity, Synapses, Time Factors, Rats, Sprague-Dawley, Long-Term Potentiation, Iron, Dietary, Rats

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