Kawamoto J C, Overmann S R, Woolley D E, Vijayan V K
Neurotoxicology. 1984 Fall;5(3):125-48.
We previously observed that lead exposure beginning at parturition reduced or retarded neuropil development and synaptogenesis in specific regions of the hippocampal formation in 15-day-old rats. To determine if morphologic effects of perinatal lead exposure persist into adulthood, the hippocampus of rats exposed to lead from parturition to weaning via the milk of dams drinking 0.2% lead acetate was analyzed by light and electron microscopy at 90-97 days of age. Preweaning lead exposure did not cause obvious hippocampal cytotoxicity, edema, damaged vasculature or altered numerical density (number per unit area) of dentate granule or hippocampal pyramidal neurons. However, lead exposure increased the area of the hilar portion of stratum pyramidale, increased the number of blood vessels per section in the dentate stratum granulosum and tended to increase the number of glial cells per section in the non-hilar CA3 stratum pyramidale. Effects of early postnatal lead exposure on synaptic profiles in the suprapyramidal mossy fiber zone (MFZ) were limited to the proximal (close to the dentate gyrus) region of the extrahilar zone. Both numerical density and areal density (proportion of neuropil covered) of complex invaginated (Ci) profiles, typical of mature mossy fiber boutons, were increased by lead exposure in the deep (close to stratum pyramidale) subfield of the proximal portion of the suprapyramidal MFZ. Lead exposure tended to increase the mean cross-sectional area of Cl profiles in the superficial (distant from stratum pyramidale) subfield of the proximal portion, and reduced the cross-sectional area of complex noninvaginated (CN) synaptic profiles in some subfields. Although lead exposure reduced or delayed neuropil development in selected late developing hippocampal regions examined at 15 days of age, it appeared to allow normal growth or to induce compensatory hypertrophy in these same regions in the adult.
我们之前观察到,从分娩开始的铅暴露会减少或延缓15日龄大鼠海马结构特定区域的神经毡发育和突触形成。为了确定围产期铅暴露的形态学影响是否会持续到成年期,我们通过光镜和电镜分析了从分娩到断奶期间通过饮用0.2%醋酸铅的母鼠乳汁而暴露于铅的大鼠在90 - 97日龄时的海马。断奶前的铅暴露未引起明显的海马细胞毒性、水肿、血管损伤或齿状颗粒神经元或海马锥体细胞的数值密度(每单位面积数量)改变。然而,铅暴露增加了锥体层门部的面积,增加了齿状颗粒层每切片的血管数量,并倾向于增加非门部CA3锥体层每切片的神经胶质细胞数量。出生后早期铅暴露对锥体上苔藓纤维区(MFZ)突触形态的影响仅限于门外部的近端(靠近齿状回)区域。在锥体上MFZ近端部分的深部(靠近锥体层)亚区,铅暴露增加了典型的成熟苔藓纤维终扣的复杂内陷(Ci)形态的数值密度和面密度(神经毡覆盖比例)。铅暴露倾向于增加近端部分浅部(远离锥体层)亚区Cl形态的平均横截面积,并减少一些亚区复杂非内陷(CN)突触形态的横截面积。尽管在15日龄时检查发现,铅暴露减少或延迟了选定的晚期发育海马区域的神经毡发育,但在成年期,这些相同区域似乎能正常生长或诱导代偿性肥大。