Beard John L, Felt Barbara, Schallert Tim, Burhans Maggie, Connor James R, Georgieff Michael K
Department of Nutrition, Penn State University, PA 16802, USA.
Behav Brain Res. 2006 Jun 30;170(2):224-32. doi: 10.1016/j.bbr.2006.02.024. Epub 2006 Mar 29.
Iron deficiency anemia in early childhood is associated with developmental delays and perhaps, irreversible alterations in neurological functioning. The goals were to determine if dietary induced gestational and lactational iron deficiency alters brain monoamine metabolism and behaviors dependent on that neurotransmitter system. Young pregnant rats were provided iron deficient or control diets from early in gestation through to weaning of pups and brain iron concentration, regional monoamine variables and achievement of specific developmental milestones were determined throughout lactation. Despite anemia during lactation, most brain iron concentrations did not fall significantly until P25, and well after significant changes in monoamine levels, transporter levels, and D2R density changed in terminal fields. The changes in D2R density were far smaller than previously observed models that utilized severe dietary restriction during lactation or after weaning. Iron deficient pups had normal birth weight, but were delayed in the attainment of a number of milestones (bar holding, vibrissae-evoked forelimb placing). This approach of iron deficiency in utero and during lactation sufficient to cause moderate anemia but not stunt growth demonstrates that monaminergic metabolism changes occur prior to profound declines in brain iron concentration and is associated with developmental delays. Similar developmental delays in iron deficient human infants suggest to us that alterations in iron status during this developmental period likely affects developing brain monaminergic systems in these infants.
幼儿期缺铁性贫血与发育迟缓相关，或许还与神经功能的不可逆改变有关。目标是确定饮食诱导的孕期和哺乳期缺铁是否会改变脑单胺代谢以及依赖于该神经递质系统的行为。从妊娠早期到幼崽断奶，给怀孕的幼鼠提供缺铁或对照饮食，并在整个哺乳期测定脑铁浓度、区域单胺变量以及特定发育里程碑的达成情况。尽管在哺乳期出现贫血，但大多数脑铁浓度直到出生后25天（P25）才显著下降，且是在终末区域单胺水平、转运体水平和D2R密度发生显著变化之后很久。D2R密度的变化远小于先前利用哺乳期或断奶后严重饮食限制的模型。缺铁幼崽出生体重正常，但在达到一些里程碑（抓杆、触须诱发前肢放置）方面有所延迟。这种子宫内和哺乳期缺铁足以导致中度贫血但不阻碍生长的方法表明，单胺能代谢变化发生在脑铁浓度大幅下降之前，且与发育迟缓有关。缺铁人类婴儿中类似的发育迟缓向我们表明，这个发育阶段铁状态的改变可能会影响这些婴儿发育中的脑单胺能系统。
