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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Iron deficiency in early development has been associated with irreversible alterations in brain myelination, but whether these neural changes are mirrored in altered behaviors in rats is not known. The goals were to determine if dietary induced gestational and lactational iron deficiency alters brain myelination and behaviors dependent on that system. Pregnant rats were randomly assigned to control (CN) or iron-deficient (ID) groups by providing iron-sufficient (40 ppm Fe) or iron-deficient (2-6 ppm Fe) diets from gestational day 5 through to weaning of pups. Thereafter, all offspring were fed the iron-sufficient diet. The myelination of subcortical white matter and the fimbria of hippocampus was measured by 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase, marker of oligodendrocyte) density at 25 days of age. Specific behavioral assessments were performed at multiple time points after birth. By contrast, ID rats had significantly lower density of CNPase in the subcortical white matter but the density of CNPase in fimbria of hippocampus was comparable to CN rats. Moreover, ID rats showed significant behavioral impairments in surface righting reflex, negative geotaxis reflex, vibrissae-evoked forelimb placing test and novel object recognition task. In conclusion, perinatal iron deficiency can significantly alter behavioral outcomes which may be due to delayed myelination in specific brain regions.
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PMID:Effect of perinatal iron deficiency on myelination and associated behaviors in rat pups. 1809 69

Developmental iron deficiency (dID) models facilitate the study of specific oligodendrocyte (OL) requirements for their progression to a mature state and subsequent contribution to myelination. In the current work, we used the dID model in transgenic mice expressing green fluorescence protein under the CNPase promoter allowing the identification of cells belonging to the oligodendroglial lineage, and the visualization of the entire myelin structure and single OL morphology. The present work evaluates dID effects on OL complexity in different brain areas. Control animals showed an increase in OL complexity both during development and along the anterior-posterior axis. In contrast, dID animals exhibited an initial increase in CNPase+ cells with prevalence of immature-OL (i-OL), an effect later compensated during development by selective death of those i-OL. As a consequence, developmental behavior was impaired in terms of body balance, muscle response, and sensorimotor functions. To explore why i-OL fail to mature in dID, expression levels of transcriptional factors involved in the maturation of the OL lineage were studied. In nuclear fractions, dID animals showed an increase in Hes5, which prevents the maturation of i-OL, and a decrease in Sox10, a positive regulator of OL maturation. The cytoplasmic fractions showed a decrease in Olig1, which is critical for precursor cell differentiation into premyelinating OL. Overall, the expression levels of Hes5, Sox10, and Olig1 in dID conditions correlated with an unfavorable OL maturation profile. In sum, the current results provide further evidence of dID impact on myelination, keeping OL away from the maturational path.
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PMID:Ontogenetic oligodendrocyte maturation through gestational iron deprivation: The road not taken. 3116 19