Heidmets Lenne-Triin, Zharkovsky Tamara, Jurgenson Monika, Jaako-Movits Kulli, Zharkovsky Alexander
University of Tartu, Department of Pharmacology, 19 Ravila Street, 51014 Tartu, Estonia.
Neurotoxicology. 2006 Jan;27(1):39-43. doi: 10.1016/j.neuro.2005.05.015. Epub 2005 Sep 15.
Although lead is widely known as a potent neurotoxin, the effect of lead exposure on the expression of the polysialic acid linked neural cell adhesion molecule (PSA-NCAM) remains unclear. We exposed Wistar rat pups to 0.2% lead acetate from postnatal day (PND) 1 to PND 30. This exposure protocol resulted in pup blood lead levels, which increased to 29.3+/-5.0 mg/dl on PND 15, and subsequently rose to 34.2+/-5.8 mg/dl at weaning. Corresponding brain tissue lead levels were 456+/-23 ng/g on PND 15 and 781+/-87 ng/g on PND 30. Animals were sacrificed on PND 80, when the blood and brain lead concentrations did not differ from those of the control group. Lead exposure induced a significant increase in the total number of PSA-NCAM expressing cells, compared to the control group (p<0.01), and did not change the proportion of cells co-expressing PSA-NCAM with glial or neuronal markers (calbindin, TuJ1, GFAP). These results suggest that early post-natal lead exposure induces persistent changes in the number of PSA-NCAM expressing cells, which could be, at least, partly the basis of impairments in the learning and memory formation, which follows low-level lead exposure.
尽管铅作为一种强效神经毒素广为人知，但铅暴露对多唾液酸连接神经细胞黏附分子（PSA-NCAM）表达的影响仍不清楚。我们从出生后第1天（PND1）至第30天给Wistar大鼠幼崽喂食0.2%的醋酸铅。这种暴露方案导致幼崽血铅水平在PND15时升至29.3±5.0mg/dl，随后在断奶时升至34.2±5.8mg/dl。相应的脑组织铅水平在PND15时为456±23ng/g，在PND30时为781±87ng/g。在PND80时处死动物，此时血铅和脑铅浓度与对照组无差异。与对照组相比，铅暴露导致表达PSA-NCAM的细胞总数显著增加（p<0.01），且不改变共表达PSA-NCAM与胶质或神经元标志物（钙结合蛋白、TuJ1、GFAP）的细胞比例。这些结果表明，出生后早期铅暴露会导致表达PSA-NCAM的细胞数量持续变化，这可能至少部分是低水平铅暴露后学习和记忆形成受损的基础。
