Iron repletion at postnatal day 8 does not correct monoamine metabolism in early iron deficient rats

Abstract

Iron deficiency in utero and in early postnatal life causes changes in brain development and associated behaviors that can extend into the individual's second decade of life. Rodent models have shown that alterations in brain monoamine metabolism due to dietary iron deficiency in early life appear to be associated with changes in neurobehavioral development. Based on earlier studies, the ideal time for iron repletion in the rat appears to be after day 4 (P4) of postnatal life and sometime before P15. In this study, rats were subjected to one of three treatments: 1) iron sufficient through gestation and lactation; 2) iron deficient beginning on G5; 3) iron deficient beginning on G5 followed by iron sufficient at P8. Although regional brain iron levels in iron repleted rats were similar to control by P21, dopamine and other monoamine levels were significantly reduced in prefrontal cortex and ventral midbrain at P21 and P90 and in striatum at P90. Monoamine‐related protein levels were also disturbed in the iron supplemented group at both time points. These results suggest that iron repletion at P8 is too late to normalize changes in brain monoamine neurotransmission caused by early life iron deficiency. Supported by NIH grant PO1‐HD39386.