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Quantitating Iron Transport Across the Mouse Placenta In Vivo Using Nonradioactive Iron Isotopes
Published on: May 10, 2022
Perinatal iron deficiency alters the neurochemical profile of the developing rat hippocampus
Raghavendra Rao1, Ivan Tkac, Elise L Townsend
1Department of. Pediatrics, University of Minnesota, Minneapolis, MN 55455, USA. raoxx017@umn.edu
Insights
Perinatal iron deficiency alters the developing rat hippocampus, impacting key metabolites related to energy, neurotransmission, and myelination. These neurochemical changes may explain cognitive deficits seen in iron-deficient infants.
Area of Science:
- Neuroscience
- Developmental Biology
- Biochemistry
Background:
- Cognitive deficits in infants at risk for perinatal iron deficiency are linked to the developing hippocampus.
- Understanding the neurochemical basis of hippocampal injury in iron deficiency is crucial.
Purpose of the Study:
- To investigate the neurochemical profile of the hippocampus in iron-deficient rats during development.
- To identify specific metabolite changes associated with perinatal iron deficiency.
Main Methods:
- Longitudinal 1H NMR spectroscopy at 9.4 T was used to quantify 16 metabolites in the rat hippocampus.
- Iron deficiency was induced in dams from gestational day 3 to postnatal day 7.
- Metabolite concentrations were measured longitudinally from postnatal day 7 to 28 in iron-deficient and iron-sufficient rats.
Main Results:
- Iron concentration in the brain was significantly lower in iron-deficient rats.
- Concentrations of phosphocreatine, glutamate, N-acetylaspartate, aspartate, gamma-aminobutyric acid, phosphorylethanolamine, and taurine were elevated in iron-deficient rats.
- The phosphocreatine/creatine ratio was also increased in the iron-deficient group.
Conclusions:
- Perinatal iron deficiency causes significant neurochemical alterations in the developing hippocampus.
- These alterations suggest disruptions in energy metabolism, neurotransmission, and myelination.
- The altered hippocampal neurochemical profile may underlie cognitive deficits observed in human infants with perinatal iron deficiency.
Abstract:
Cognitive deficits in human infants at risk for gestationally acquired perinatal iron deficiency suggest involvement of the developing hippocampus. To understand the plausible biological explanations for hippocampal injury in perinatal iron deficiency, a neurochemical profile of 16 metabolites in the iron-deficient rat hippocampus was evaluated longitudinally by 1H NMR spectroscopy at 9.4 T. Metabolites were quantified from an 11-24 microL volume centered in the hippocampus in 18 iron-deficient and 16 iron-sufficient rats on postnatal day (PD) 7, PD10, PD14, PD21 and PD28. Perinatal iron deficiency was induced by feeding the pregnant dam an iron-deficient diet from gestational d 3 to PD7. The brain iron concentration of the iron-deficient group was 60% lower on PD7 and 19% lower on PD28 (P < 0.001 each). The concentration of 12 of the 16 measured metabolites changed over time between PD7 and PD28 in both groups (P < 0.001 each). Compared with the iron-sufficient group, phosphocreatine, glutamate, N-acetylaspartate, aspartate, gamma-aminobutyric acid, phosphorylethanolamine and taurine concentrations, and the phosphocreatine/creatine ratio were elevated in the iron-deficient group (P < 0.02 each). These neurochemical alterations suggest persistent changes in resting energy status, neurotransmission and myelination in perinatal iron deficiency. An altered neurochemical profile of the developing hippocampus may underlie some of the cognitive deficits observed in human infants with perinatal iron deficiency.
