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Early iron deficiency alters sensorimotor development and brain monoamines in rats
Erica L Unger1, Tessy Paul, Laura E Murray-Kolb
1Department of Nutrition Sciences, The Pennsylvania State University, University Park, PA 16802, USA.
Insights
Prenatal iron deficiency in rats delayed development and altered dopamine systems. Postnatal iron deficiency also caused developmental delays and reduced dopamine, showing critical impacts of iron during early life.
Area of Science:
- Neuroscience
- Developmental Biology
- Nutritional Science
Background:
- Iron deficiency in infancy is linked to irreversible developmental delays and neurobiological changes.
- Understanding the precise timing and impact of iron deficiency on early development is crucial.
Purpose of the Study:
- To investigate the effects of prenatal and postnatal iron deficiency on sensorimotor development and brain monoaminergic systems in a rodent model.
- To determine the impact of iron deficiency initiated at different developmental stages (gestational day 15 and postnatal day 4) on neurodevelopment.
Main Methods:
- Rats were subjected to four dietary treatments: iron-sufficient control, prenatal iron deficiency (G15), postnatal iron deficiency (P4), and combined prenatal/postnatal iron deficiency.
- Evaluated developmental milestones, open field behavior, brain iron, proteins, monoamines, and transporters from postnatal day 6 to 21.
Main Results:
- Prenatal iron deficiency (G15) increased dopaminergic activity, tyrosine hydroxylase, and dopamine levels in the prefrontal cortex and striatum.
- Prenatal iron deficiency led to delayed eye opening, ear development, and reduced locomotor activity.
- Postnatal iron deficiency (P4) reduced iron and dopamine levels and caused developmental delays in ear development, bar holding, and surface righting.
Conclusions:
- Iron deficiency initiated during late gestation significantly impacts early dopamine neurobiology, sensorimotor milestones, and behavior in developing rats.
- Iron repletion can partially reverse some effects of prenatal iron deficiency.
- Both prenatal and postnatal iron deficiency negatively affect neurodevelopment and sensorimotor function, highlighting the critical role of iron during early life stages.
Abstract:
Iron deficiency in human infancy reportedly leads to developmental delays and changes in neurobiology that may be irreversible. Using a rodent model, the present study examined whether dietary iron deficiency late in pregnancy and during lactation alters sensorimotor development and brain monoaminergic systems. Rats were assigned to 1 of 4 dietary treatments during gestation and lactation: 1) iron sufficient control; 2) prenatal iron deficiency beginning on gestational d 15 (G15); 3) postnatal iron deficiency beginning on postnatal d 4 (P4); 4) iron deficiency beginning on G15 followed by an iron sufficient diet on P4. Developmental milestones, open field behavior, brain iron and proteins, monoamines, and their transporters were evaluated between P6 and P21. Only G15 iron deficient rats had greater dopaminergic activity than controls as indicated by increased tyrosine hydroxylase levels, phosphorylated tyrosine hydroxylase levels, and cellular dopamine in prefrontal cortex and striatum at P15. These rats also showed delayed eye opening, ear development, and reduced locomotor activity. Iron repletion at P4 returned most measures to control levels by the time of weaning. Postnatal iron deficiency reduced striatal and ventral midbrain iron as well as cellular dopamine levels in prefrontal cortex and striatum at P21. Developmental delays in ear development and achievement in bar holding and surface righting also resulted from postnatal iron deficiency. These results indicate that iron deficiency begun at G15 affects early dopamine neurobiology, the development of specific developmental milestones, and behavior in preweaned rats.
