Morphometric and enzymatic effects of neonatal lead exposure in the rat brain

Abstract

Lead acetate (7.5 mg/kg ip) was administered to rat pups from birth to 10 days of age. This dose did not impair weight gain or produce overt signs of lead toxicity. The animals were sacrificed at 10, 15, 20, or 30 days of age for enzymatic analysis or morphometric assessment. Thickness of the pyramidal cell layer of the hippocampal formation and of the granular cell layer of the dentate gyrus was measured. The activity of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) was determined in homogenates from separate brain regions. Significant ( p < 0.05) reductions of AChE activity were produced at 10 days in the hippocampus (40%) and medulla oblongata (17%). Although cerebral AChE was reduced by 17%, the reduction of hippocampal AChE (32%) was not significant nor were decreases in AChE observed in either the cerebellum, midbrain, corpus striatum, or medulla oblongata of 20-day-old lead-treated rats. No inhibition of BuChE activity was observed at 10 days. However, BuChE of the midbrain, hippocampus, and cerebrum of 15-day-old animals was decreased by 32, 37, and 12%, respectively. Similrly, BuChE activity of homogenates from the cerebrum, hippocampus, and midbrain of 20-day-old lead-treated rats was reduced by 35, 35, and 37%, respectively. No significant decreases in AChE or BuChE activity were produced in brain homogenates from 30-day-old animals. Measurements of hippocampal cell layer thickness and distance from the hippocampus to the cerebral cortex indicated that lead administration produced 10–15% reductions in both parameters. The results suggest that lead exposure may produce a reversible impairment of AChE and BuChE in specific brain regions of the developing rat brain. However, morphological effects of lead exposure may persist after the effects on BuChE and AChE activities are no longer discernible.