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Pre- and postweaning iron deficiency alters myelination in Sprague-Dawley rats
John L Beard1, Jason A Wiesinger, James R Connor
1Nutrition Sciences, Integrative Biosciences Graduate Program, Pennsylvania State University, S 126 Henderson Building, University Park, PA 16802, USA. jbeard@psu.edu
Insights
Postnatal iron deficiency, even for short periods, impairs myelin production and oligodendrocyte function. This effect persists even when iron deficiency occurs after the critical early development period, impacting myelin maintenance.
Area of Science:
- Neuroscience
- Developmental Biology
- Nutritional Science
Background:
- Iron deficiency in early life is linked to hypomyelination.
- The precise role of iron in myelinogenesis remains unclear.
Purpose of the Study:
- To investigate the impact of preweaning and postweaning iron deficiency on myelin development markers.
- To assess the effects of iron deficiency on oligodendrocyte metabolic activity and myelin basic protein concentrations.
Main Methods:
- Rats were subjected to iron deficiency during preweaning (PND 4-14, PND 4-21) and postweaning (PND 21-63) periods.
- Assessed 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase) activity and myelin basic protein (MBP) concentrations in the cerebrum and hindbrain.
- Analyzed hindbrain fatty acid composition of phospholipids and cytochrome oxidase activities.
Main Results:
- Iron deficiency significantly reduced CNPase activity and MBP concentrations in both cerebrum and hindbrain across all tested groups.
- MBP concentrations decreased by 25-35% in iron-deficient animals.
- Alterations in hindbrain phospholipid fatty acid composition and cytochrome oxidase activities were observed.
Conclusions:
- Postnatal iron deficiency, even for brief durations (10 days), significantly impairs myelin production and oligodendrocyte function.
- Iron deficiency during postweaning periods also negatively affects CNPase activity and MBP concentrations, suggesting an impact on myelin maintenance.
- These findings highlight the critical role of iron in both the development and maintenance of myelin throughout postnatal life.
Abstract:
Iron deficiency in early life is associated with hypomyelination; however, the role which iron plays in myelinogenesis is not clearly established. In this study, we examined the effect of preweaning [postnatal days (PND) 4-14 and PND 4-21] and postweaning (PND 21-63) iron deficiency on hindbrain 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase) activity (marker of oligodendrocyte metabolic activity) and myelin basic protein (MBP) concentrations. Both CNPase activity and concentrations in the cerebrum and hindbrain were significantly lower in pre- and postweaning iron-deficient rats. Similarly, MBP concentrations were also reduced (25-35%) in all three groups of iron-deficient animals. Iron-deficient animals also had significant alterations in the fatty acid composition of individual phospholipids within the hindbrain as well as changes in cytochrome oxidase activities. These studies show that postnatal iron deficiency, for as little as 10 days, can significantly alter the production of myelin and oligodendrocyte functioning. Importantly, postweaning iron deficiency was still associated with a decrease in CNPase activity and MBP concentrations despite occurring well past a likely key sensitive period of peak myelinogenesis at PND 8-12. This suggests that iron deficiency in later life, as well as during early postnatal growth, can effect the production and maintenance of myelin.
