ABSTRACT
In humans, iron deficiency early in life produces persistent, impaired cognition. Dietary iron replacement does not ameliorate these problems and to date, no attempt to treat these individuals pharmacologically has been reported. The aim of this work was to test the hypothesis that rats made iron deficient in early infancy exhibit cognitive deficits similar to those seen in humans at adolescence. A second aim was to investigate whether the deficit could be treated pharmacologically. Sprague-Dawley rats were made iron deficient (ID) starting at postnatal day 4 by being placed with iron-deficient dams (vs. control). At weaning, all pups were placed on an iron-sufficient diet for the remainder of the study. At 45 days of age, the animals were tested for attention set shifting. After testing, the animals were assigned to one of three methylphenidate (MePh) dose groups, 1, 5 or 10 mg/kg, p.o., vs. vehicle control and treated daily for 15 days prior to a second round of attention set shift testing and continued throughout testing. The results showed that ID rats performed more poorly than controls overall on attentional set-shift testing. MePh improved ID rats' performance and lower doses were more effective than higher doses. This is the first demonstration that MePh can improve cognitive deficits produced by early ID in animals. These findings may open the possibility of pharmacotherapy to treat the persistent cognitive difficulties in children who were severely iron deficient in early infancy.
