Campbell J B, Woolley D E, Vijayan V K, Overmann S R
Brain Res. 1982 Apr;255(4):595-612. doi: 10.1016/0165-3806(82)90056-6.
Neurotoxic sequelae of developmental lead exposure suggest that the hippocampus may be affected. Therefore, rats received low-level exposure via the milk of dams drinking 0.2% lead acetate beginning at parturition, and mid-dorsal sections of the hippocampus and dentate gyrus (DG) from 15-day-old pups were examined by light and electron microscopy. Lead exposure did not reduce body weight nor produce obviously abnormal vascularity or signs of cytotoxicity in the hippocampal formation, and total numbers per section of dentate granule cells or CA3 pyramidal cells were not reduced. On the other hand, lead exposure reduced neuropil development as evidenced both by reduced areas of the dentate hilus and dentate infrapyramidal stratum moleculare and by increased number of hilar CA3 pyramidal cells per unit area. Also, lead exposure reduced numbers of several types of synaptic profiles per unit area in the suprapyramidal mossy fiber zone. Complex invaginated (CI) profiles, assumed to be mature mossy fiber boutons, were characterized by multiple membrane densities and deep invaginations around dendritic spines of pyramidal cells. Complex noninvaginated (CN) boutons exhibited bag-like profiles with multiple membrane densities. Smaller, less numerous, simple (S) profiles contacted either dendritic trunks (ST) or spines (SS). Lead exposure reduced the numerical density of any of the profiles in the deep (close to stratum pyramidale) part of the proximal (close to DG) region of the suprapyramidal mossy fiber zone, but did not alter the numerical density of any of the profiles in the superficial (distal to stratum pyramidale) parts of either proximal or distal (close to CA1) regions. Average size of CN profiles in the distal region was increased by lead exposure. The pattern of effects suggests that low-level lead exposure during development preferentially affects later developing structures within the hippocampal formation, rather than affecting mature structures.
发育过程中铅暴露的神经毒性后遗症表明海马体可能会受到影响。因此,从分娩开始,让大鼠通过饮用含0.2%醋酸铅的母鼠乳汁接受低水平铅暴露,并对15日龄幼鼠海马体和齿状回(DG)的中背部切片进行光镜和电镜检查。铅暴露并未降低体重,也未在海马结构中产生明显异常的血管生成或细胞毒性迹象,并且每切片中齿状颗粒细胞或CA3锥体细胞的总数并未减少。另一方面,铅暴露减少了神经毡的发育,这在齿状门和齿状锥体下分子层面积减少以及每单位面积门区CA3锥体细胞数量增加中得到了体现。此外,铅暴露减少了锥体上苔藓纤维区每单位面积几种类型突触轮廓的数量。复杂内陷(CI)轮廓被认为是成熟的苔藓纤维终扣,其特征是在锥体细胞树突棘周围有多个膜密度和深内陷。复杂非内陷(CN)终扣呈现出具有多个膜密度的袋状轮廓。较小、数量较少的简单(S)轮廓与树突干(ST)或树突棘(SS)接触。铅暴露降低了锥体上苔藓纤维区近端(靠近DG)区域深部(靠近锥体层)部分中任何一种轮廓的数值密度,但并未改变近端或远端(靠近CA1)区域浅表(远离锥体层)部分中任何一种轮廓的数值密度。铅暴露使远端区域CN轮廓的平均大小增加。这种效应模式表明,发育过程中的低水平铅暴露优先影响海马结构中较晚发育的结构,而非成熟结构。