Chronic prenatal lead exposure impairs long-term memory in day old chicks

Environmental exposure to lead during developmental stages has been established as a potential cause of intellectual deficits. The high susceptibility of rapidly developing fetal and infant brains to external factors suggests that impairment of later cognitive functions may arise from relatively minor prenatal exposure to environmental lead levels. In this study, we used the one-trial passive avoidance learning paradigm with day old chicks to evaluate memory function and memory consolidation in response to prenatal lead exposure. Lead acetate (5.5mg/kg, 11mg/kg, 16.5mg/kg) was administered daily from E9 to E16 via direct injection into the airspace in chick eggs. Higher doses of lead acetate (11mg/kg, 16.5mg/kg) administration had significant effects on the hatching success (23.4 and 17, respectively) and hatch weight ( approximately 10% decrease) of chicks when compared to equivalent treatments of sodium acetate (11mg/kg, 16.5mg/kg) (p<0.001). Low doses of lead acetate (5.5mg/kg) did not significantly affect chick hatching, weight or morphology compared to equivalent sodium acetate treatments (5.5mg/kg) and controls. However, lead acetate (5.5mg/kg) was found to significantly impair long-term memory after 120min following training in the one-trial passive avoidance learning task (p<0.05). These findings add to a growing body of evidence that suggests lead toxicity during fetal development leads to impairment in cognitive and memory processes.