The objective of this study was to investigate the effects of lead exposure on spatial learning and memory capacity and the expression of amyloid β and phosphorylated tau proteins in the mouse hippocampus. A total of 24 adult C57BL/6 mice (12 of each sex) were mated at a 1:1 ratio. After delivery, the litters were normalised to 6 pups per litter. During the lactation period, the pups were randomly separated into four groups: control, early exposure, late exposure, or long-term exposure. These groups were not exposed to lead, exposed to lead from birth to week 24, exposed to lead from week 24 to week 48, or exposed to lead from birth to 48 weeks of age, respectively. Lead exposure was induced by providing Pb-contaminated drinking water at a concentration of 0.1%. All of the pups were fed until 72 weeks of age, at which time their spatial learning and memory capacity was evaluated via the Morris water maze test. Then, the lead levels in their blood and hippocampus were measured via graphite furnace atomic absorption spectrometry. The protein expression of amyloid β and phosphorylated tau in the hippocampus was detected via Western blot. The results revealed that the hippocampal and blood lead levels were significantly higher in all of the groups exposed to lead than the control group (P<0.05). The spatial learning and memory performances of the lead-exposed groups were much poorer than those of the control group (P<0.05). The expression levels of amyloid β and phosphorylated tau proteins were increased in the lead-exposed groups compared to the control group (P<0.05). The enhanced expressions of amyloid β and phosphorylated tau proteins might contribute to the impairment in spatial learning and memory in the lead-exposed mice.
Keywords: Amyloid β; Lead; Learning and memory; Neurotoxicity; Phosphorylated tau protein.
Copyright © 2014. Published by Elsevier GmbH.