Takeda M, Tatebayashi Y, Tanimukai S, Nakamura Y, Tanaka T, Nishimura T
Department of Neuropsychiatry, Osaka University Medical School, Japan.
Acta Neuropathol. 1991;82(5):346-52. doi: 10.1007/BF00296545.
Experimental neurofibrillary change was produced in rabbit brain by daily subcutaneous aluminum tartrate injection for 40 days. The production of experimental neurofibrillary changes was confirmed by immunostaining with antibodies against neurofilament triplet proteins and the brain tissue was studied immunohistochemically with antibodies against microtubule-associated protein (MAP) 2 and ubiquitin. The hippocampal neurons of the chronically aluminum-intoxicated rabbit brain showed diminished staining of dendrites by anti-MAP2 antibody. The length of anti-MAP2-positive dendrites in hippocampus was significantly shorter than that of the control brain. In the cortex somata of a subset of pyramidal neurons were intensively stained by anti-MAP2 antibody, while the MAP2 immunoreactivity of distal dendrites was diminished. The immunostaining by anti-ubiquitin antibody revealed the positive staining of the neurons bearing experimental neurofibrillary changes in the lower brain stem nuclei. It is speculated that MAP2 dislocation and ubiquitination are accompanying phenomena of the production of experimental neurofibrillary changes in chronically aluminum-intoxicated rabbit brains.
通过每天皮下注射酒石酸铝40天,在兔脑中产生实验性神经原纤维变化。用抗神经丝三联体蛋白抗体进行免疫染色证实了实验性神经原纤维变化的产生,并用抗微管相关蛋白(MAP)2和泛素的抗体对脑组织进行免疫组织化学研究。长期铝中毒兔脑的海马神经元显示抗MAP2抗体对树突的染色减弱。海马中抗MAP2阳性树突的长度明显短于对照脑。在皮质中,一部分锥体神经元的胞体被抗MAP2抗体强烈染色,而远端树突的MAP2免疫反应性减弱。抗泛素抗体的免疫染色显示,在脑桥下部核中,具有实验性神经原纤维变化的神经元呈阳性染色。推测MAP2错位和泛素化是长期铝中毒兔脑实验性神经原纤维变化产生的伴随现象。