Kadish Inga, Pradier Laurent, van Groen Thomas
Department of Neuroscience and Neurology, University of Kuopio, FIN 70211 Kuopio, Finland.
Brain Res Bull. 2002 Mar 15;57(5):587-94. doi: 10.1016/s0361-9230(01)00751-1.
We have examined the effects of the presence of the mutated human presenilin 1 gene (M146L; hps1*) on lesion-induced sprouting in the hippocampus of the mouse (C57/CBA). The entorhinal cortex was unilaterally lesioned with ibotenic acid in adult, male mice. Four weeks later the subsequent axonal sprouting in the dentate gyrus was analysed, by measuring the density of the synaptophysin immunocytochemical staining in the termination area of the entorhinal cortex axons. The data demonstrate that mice expressing either the human presenilin 1 gene (hps1) or the hps1* gene display a significantly increased density of immunocytochemical staining for synaptophysin, indicative of axonal sprouting, compared to the control mice. No (or a very small) sprouting response is observed in mice expressing the normal mouse ps1 gene. Taken together, these data indicate that the presence of a human ps1 gene, normal or with an Alzheimer's disease mutation, leads to enhanced plasticity in the mouse brain.
我们研究了突变的人类早老素1基因（M146L；hps1*）的存在对小鼠（C57/CBA）海马体中损伤诱导的轴突发芽的影响。在成年雄性小鼠中，用鹅膏蕈氨酸单侧损伤内嗅皮质。四周后，通过测量内嗅皮质轴突终末区域中突触素免疫细胞化学染色的密度，分析齿状回中随后的轴突发芽情况。数据表明，与对照小鼠相比，表达人类早老素1基因（hps1）或hps1*基因的小鼠突触素免疫细胞化学染色密度显著增加，表明有轴突发芽。在表达正常小鼠ps1基因的小鼠中未观察到（或仅有非常小的）发芽反应。综上所述，这些数据表明，人类ps1基因的存在，无论是正常的还是带有阿尔茨海默病突变的，都会导致小鼠大脑可塑性增强。
