Abnormal motor function persists following recovery from perinatal copper deficiency in rats.

What are the biochemical and behavioral consequences of perinatal copper deficiency? Pregnant Holtzman rats were fed a modified AIN-76A diet low in copper (0.34 mg Cu/kg and 42 mg Fe/kg) starting on gestation d 7. Seven rats received copper in their drinking water (20 mg Cu/L) (+Cu) and 7 drank deionized water (-Cu). Treatments did not affect litter size or pregnancy outcome. Compared with +Cu dams and a sample of +Cu male weanling [postnatal day (P)21] offspring, -Cu rats exhibited signs consistent with copper deficiency. P21 males were switched to a nonpurified copper-adequate diet and sampled biochemically after 3 mo and behaviorally after 3 and 6 mo of repletion (CuR). Compared with controls, CuR rats had lower brain copper and iron levels 3 and 6 mo after repletion; other biochemical differences were not detected. Behavioral assessments after 5 mo of repletion indicated a persistent impairment in motor function of CuR compared with control rats as evaluated by the accelerating rotorod procedure. These results suggest that permanent impairment to motor function can persist after long-term recovery from perinatal copper deficiency.