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Cited by 200Iron Metabolism and DisordersNeurogenesis and neuroplasticity mechanismsTrace Elements in Health

Pre- and postweaning iron deficiency alters myelination in Sprague-Dawley rats

Beard, John L., Wiesinger, Jason A., Connor, James R.·2003·Developmental Neuroscience
DOI 10.1159/000073507
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Abstract

Iron deficiency in early life is associated with hypomyelination; however, the role which iron plays in myelinogenesis is not clearly established. In this study, we examined the effect of preweaning [postnatal days (PND) 4–14 and PND 4–21] and postweaning (PND 21–63) iron deficiency on hindbrain 2′,3′-cyclic nucleotide 3′-phosphohydrolase (CNPase) activity (marker of oligodendrocyte metabolic activity) and myelin basic protein (MBP) concentrations. Both CNPase activity and concentrations in the cerebrum and hindbrain were significantly lower in pre- and postweaning iron-deficient rats. Similarly, MBP concentrations were also reduced (25–35%) in all three groups of iron-deficient animals. Iron-deficient animals also had significant alterations in the fatty acid composition of individual phospholipids within the hindbrain as well as changes in cytochrome oxidase activities. These studies show that postnatal iron deficiency, for as little as 10 days, can significantly alter the production of myelin and oligodendrocyte functioning. Importantly, postweaning iron deficiency was still associated with a decrease in CNPase activity and MBP concentrations despite occurring well past a likely key sensitive period of peak myelinogenesis at PND 8–12. This suggests that iron deficiency in later life, as well as during early postnatal growth, can effect the production and maintenance of myelin.

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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 [56]

  • 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 [56]

  • 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 [56]

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Authors
Beard, J. L., Wiesinger, J. A., & Connor, J. R.
Affiliations
Pennsylvania State University (US)
ORCID
Venue
Developmental Neuroscience
Publisher
S. Karger AG
Published
2003
Volume
25
Issue
5
Pages
308-315
ISSN
  • 0378-5866 (ISSN-L)
  • 1421-9859
DOI
10.1159/000073507
OpenAlex
W1970461946
Cited by
200
References
31
Citations by year
2026: 4 · 2025: 6 · 2024: 13 · 2023: 6 · 2022: 6 · 2021: 5 · 2020: 4 · 2019: 12 · 2018: 11 · 2017: 5 · 2016: 6 · 2015: 11 · 2014: 9 · 2013: 11 · 2012: 10
FWCI
3.41
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Developmental Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01ns034280-04)
  • National Institute of Neurological Disorders and Stroke (NS34280)
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
iron deficiency, myelination, myelin basic protein, CNPase, oligodendrocytes, postnatal development, phospholipid fatty acid composition, cytochrome c oxidase, hindbrain, cerebrum
MeSH terms
Iron Deficiencies, Age Factors, Animals, Animals, Suckling, Brain, Brain Chemistry, Electron Transport Complex IV, Diet, Myelin Basic Protein, Enzyme-Linked Immunosorbent Assay, Female, Immunohistochemistry, Male, Myelin Sheath, Phospholipids, Tyrosine 3-Monooxygenase, Weaning, 2',3'-Cyclic-Nucleotide Phosphodiesterases, Rats, Sprague-Dawley, Rats

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