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

The hippocampus is especially sensitive to the effects of gestational and neonatal iron deficiency, even after iron repletion. This study compared the effects of iron deficiency, maintained from gestational day 2 to postnatal day (P)7, on "delay" and "trace" fear conditioning. Only the latter paradigm is critically dependent on the dorsal hippocampus. In different groups of rats, fear conditioning commenced either prior to puberty (P28 or P35) or after puberty (P56). Fear conditioning was measured using fear-potentiated startle. Both delay and trace fear conditioning were diminished by iron deficiency at P28 and P35. Hippocampal expression of the plasticity-related protein PKC-gamma was increased through trace fear conditioning, but reduced at P35 in the iron-deficient group. Trace fear conditioning was enhanced by prior iron deficiency in the P56 group. This unanticipated finding in iron-repleted adults is consistent with the effects of developmental iron deficiency on inhibitory avoidance learning, but contrasts with the persistent deleterious long-term effects of a more severe iron-deficiency protocol, suggesting that degree and duration of iron deficiency affects the possibility of recovery from its deleterious effects.
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PMID:Effects of gestational iron deficiency on fear conditioning in juvenile and adult rats. 1878 13

Fetal and neonatal iron deficiency results in cognitive impairments in adulthood despite prompt postnatal iron replenishment. To systematically determine whether abnormal expression and localization of proteins that regulate adult synaptic efficacy are involved, we used a quantitative proteomic approach (isobaric tags for relative and absolute quantitation, iTRAQ) and pathway analysis to identify dysregulated proteins in hippocampal synapses of fetal iron deficiency model. Rat pups were made iron deficient (ID) from gestational day 2 through postnatal day (P) 7 by providing pregnant and nursing dams an ID diet (4 ppm Fe) after which they were rescued with an iron-sufficient diet (200 ppm Fe). This paradigm resulted in a 40% loss of brain iron at P15 with complete recovery by P56. Synaptosomes were prepared from hippocampi of the formerly iron-deficient (FID) and always iron-sufficient controls rats at P65 using a sucrose gradient method. Six replicates per group that underwent iTRAQ labeling and LC-MS/MS analysis for protein identification and comparison elucidated 331 differentially expressed proteins. Western analysis was used to confirm findings for selected proteins in the glutamate receptor signaling pathway, which regulates hippocampal synaptic plasticity, a cellular process critical for learning and memory. Bioinformatics were performed using knowledge-based Interactive Pathway Analysis. FID synaptosomes show altered expression of synaptic proteins-mediated cellular signalings, supporting persistent impacts of fetal iron deficiency on synaptic efficacy, which likely cause the cognitive dysfunction and neurobehavioral abnormalities. Importantly, the findings uncover previously unsuspected pathways, including neuronal nitric oxide synthase signaling, identifying additional mechanisms that may contribute to the long-term biobehavioral deficits.
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PMID:Fetal iron deficiency alters the proteome of adult rat hippocampal synaptosomes. 2753 57