Bâ Abdoulaye, N'Douba Valentin, D'Almeida Marie-Anne, Seri Bialli Victor
University of Cocody, UFR Biosciences, Abidjan, Ivory Coast.
Acta Neurobiol Exp (Wars). 2005;65(4):387-98. doi: 10.55782/ane-2005-1567.
To understand the implication of thiamine deficiency in the neuronal atrophy and cell death we undertook to induce thiamine (B1 vitamine) deficiency during three essential periods of the ontogenesis of rat central nervous system (CNS). Female rats were fed with a thiamine deprived diet during the gestation and lactation, and the fetuses and pups were alternately exposed to prenatal, perinatal or postnatal thiamine deficiencies. On the 45th postnatal day, histological studies were done on the brains of the pups and the structure of the hippocampus was analyzed. The effects of each treatment were assessed by measuring the size and the density of cell nuclei throughout the dentate gyrus and fields CA4, CA3 and CA1 of the hippocampal formation. The hippocampus showed a regional vulnerability in the pups exposed to maternal thiamine deficiencies. It appears that the thiamine deficiency decreased nuclear density (27.20%) more severely than nuclear size (10.56%) in the fetal hippocampus. Consequently, the major part of the teratogenic effects of thiamine deficiency was cellular death, rather than cellular atrophy.
为了解硫胺素缺乏在神经元萎缩和细胞死亡中的影响,我们在大鼠中枢神经系统(CNS)个体发育的三个关键时期诱导硫胺素(维生素B1)缺乏。雌性大鼠在妊娠和哺乳期喂食缺乏硫胺素的饮食,胎儿和幼崽交替暴露于产前、围产期或产后硫胺素缺乏。在出生后第45天,对幼崽的大脑进行组织学研究,并分析海马体的结构。通过测量整个齿状回以及海马结构的CA4、CA3和CA1区细胞核的大小和密度来评估每种处理的效果。在暴露于母体硫胺素缺乏的幼崽中,海马体表现出区域易损性。似乎硫胺素缺乏对胎儿海马体细胞核密度(27.20%)的降低比细胞核大小(10.56%)更严重。因此,硫胺素缺乏的致畸作用主要是细胞死亡,而非细胞萎缩。