In order to determine whether iron sequestered by the rat brain during the third week of postnatal life could be mobilized by subsequent dietary iron deficiency (ID), iron-59 (59Fe) was administered to rats at 2 weeks of age. The animals were placed on an ID or a control diet from age 4 through 8 weeks and killed by perfusion. Brain radioactivity was identical for both groups, and autoradiography revealed no differences in the distribution of radioactivity. Thus, neither the sequestration of cerebral iron acquired at age 2 weeks nor its subsequent redistribution was affected by ID. Since ID beginning after age 3 weeks reportedly produces a cerebral iron deficit that is in part reversible, an attempt was made to determine whether 59Fe administered after ID was preferentially delivered to any brain region. Rats were placed on an ID or a control diet from age 3 through 7 weeks and then injected with 59Fe, placed on a normal diet, and killed 2 weeks later. Thre was no difference between groups in amount or distribution of brain 59Fe, except in the choroid plexus, which was more radioactive in the ID rats than in the controls. This finding may represent a mechanism by which the choroid plexus buffers the brain against rapid rises in plasma iron content.