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Objective Perinatal iron deficiency results in persistent hippocampus-based cognitive deficits in adulthood despite iron supplementation. The objective of the present study was to determine the long-term effects of perinatal iron deficiency and its treatment on hippocampal anatomy and neurochemistry in formerly iron-deficient young adult rats. Methods Perinatal iron deficiency was induced using a low-iron diet during gestation and the first postnatal week in male rats. Hippocampal size was determined using volumetric magnetic resonance imaging at 8 weeks of age. Hippocampal neurochemical profile, consisting of 17 metabolites indexing neuronal and glial integrity, energy reserves, amino acids, and myelination, was quantified using high-field in vivo 1H NMR spectroscopy at 9.4 T (N = 11) and compared with iron-sufficient control group (N = 10). Results The brain iron concentration was 56% lower than the control group at 7 days of age in the iron-deficient group, but had recovered completely at 8 weeks. The cross-sectional area of the hippocampus was decreased by 12% in the formerly iron-deficient group (P = 0.0002). The hippocampal neurochemical profile was altered: relative to the control group, creatine, lactate, N-acetylaspartylglutamate, and taurine concentrations were 6-29% lower, and glutamine concentration 18% higher in the formerly iron-deficient hippocampus (P < 0.05). Discussion Perinatal iron deficiency was associated with reduced hippocampal size and altered neurochemistry in adulthood, despite correction of brain iron deficiency. The neurochemical changes suggest suppressed energy metabolism, neuronal activity, and plasticity in the formerly iron-deficient hippocampus. These anatomic and neurochemical changes are consistent with previous structural and behavioral studies demonstrating long-term hippocampal dysfunction following perinatal iron deficiency. [ABSTRACT FROM AUTHOR]

Abstract: Early iron deficiency (ID) is one of the most common nutrient deficiencies in both developed and developing countries. This condition has been linked to perturbations in myelin formation, alterations of monoamine neurotransmitter systems particularly in the striatum, and deficits in energy metabolism particularly in the hippocampus (HP) and prefrontal cortex (PFC) in rats. Early ID has also been traced to long-term behavioral consequences in children in domains linked to these neuropathologies. The current experiment assesses formerly iron deficient (FID) adult rats on a delayed alternation (DA) task — a procedure thought to be sensitive to PFC dysfunction. Rat dams were started on an iron deficient chow at gestational day (G) 2 and maintained on this diet until postnatal day (P) 7; behavioral training began at P 65 when animals were iron replete. FID animals exhibited accelerated acquisition (p=0.002) and fewer errors (p=0.003) on the DA task compared to controls. These findings may reflect an imbalance between hippocampal and prefrontal modulation of this behavior most likely emanating from long-term hippocampal disinhibition by early ID that persists in spite of early iron treatment from P 7. [ABSTRACT FROM AUTHOR]

Iron deficiency (ID) is a common nutrient deficiency worldwide. This condition is linked to changes in myelin formation, dopaminergic function, and energy metabolism. Early ID results in persistent long-term cognitive and behavioral disturbances in children, despite a return to normal iron status. The present study assesses formerly ID adult rats on maze learning tasks that depend on specific brain regions related to learning, specifically the hippocampus, striatum, and amygdala. Rat dams were fed ID chow starting on gestational Day 2 through postnatal Day 7, and behavioral testing began at postnatal Day 65-following a return to normal iron status. Formerly ID rats exhibited delayed acquisition of the hippocampus-dependant task and no differences from controls on the striatum- and amygdala-dependent tasks. These findings likely reflect long-term reduction in but not abolition of hippocampus-dependent learning and preserved function in other brain structures (e.g., striatum and amygdala). [ABSTRACT FROM AUTHOR]