Dietary iron deficiency (ID) targets the striatum, a brain area involved in procedural memory. Fetal ID is a known risk of gestational diabetes and intrauterine growth retardation. We evaluated the effects of fetal ID on (1) biochemically important metabolites in the striatum in vivo and concomitant (2) striatally based behaviors. Absolute metabolite concentrations from a striatally centered 10-13 μL volume were measured serially by ultra-short echo-time 1 H nuclear magnetic resonance (NMR) spectroscopy at 9.4 Tesla and LC Model processing in 10 ID and 10 control rats on postnatal days (P) 8, 22 (peak anemia), and 37 (post-anemia). An established model of moderate fetal/neonatal ID was used. All 13 metabolites and two ratios changed over time in both groups (p ≤ .005), confirming a developmental trajectory. ID and IS groups differed in 7 metabolites [phosphocreatine (PCr), p = .03; glucose (Glc), taurine (Tau), N-acetylaspartate (NAA), glutamine (Gln) and inositol (Ins), and lactate (Lac), all p < .002]. There was an age by diet effect for GABA (p = .016), Glc (p = .004), creatine (Cr), glutamate (Glu), and Ins (all p ≤ .001), NAA (p = .044), and Tau (p = .007). Behavior performances also showed developmental trajectories in both groups (p < .001), but the ID group demonstrated an age by diet interaction (p ≤ .001). Behavioral performance at P22 was best predicted by striatal concentrations of Glc, Glu, NAA, Ins, and Gln (bilateral forelimb placing, r = .86, p < .002; right vibrissae-evoked forelimb placing, r = .79, p = .016; left vibrissae-evoked forelimb placing, r = .91, p ≤ .001). Early ID alters striatal bioenergetic (PCr, Cr, Glc, and Lac), neurotransmitter (Glu, GABA, and Tau), and myelin (Gln, Ins, and NAA) metabolites, potentially altering striatally based behaviors.
Supported by NIH grant # HD-39386.
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