Kitamura Y, Zhao X H, Ohnuki T, Nomura Y
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.
Neurosci Lett. 1989 Dec 4;106(3):334-8. doi: 10.1016/0304-3940(89)90186-9.
The senescence accelerated mouse (SAM) is known as a murine model of aging and memory dysfunction. In the cerebral cortical membranes of male 9-month-old SAM mice, the Bmax values of [3H]rauwolscine and [3H]nitrendipine binding, and the values of both Kd and Bmax of [3H]TCP binding in the accelerated aging strain SAM-P/8, were significantly increased compared with the values in the control strain SAM-R/1. In hippocampal membranes, however, the Bmax values of [3H]quinuclidinyl benzilate and [3H]nitrendipine binding were significantly decreased in SAM-P/8 compared with those in SAM-R/1. These results suggest that muscarinic acetylcholine receptors, alpha 2-adrenoceptors, N-methyl-D-aspartate receptor channels and L-type Ca2+ channels are changed in cerebral cortex and hippocampus in SAM-P/8 at 9 months.
衰老加速小鼠(SAM)是一种已知的衰老和记忆功能障碍的小鼠模型。在9个月大的雄性SAM小鼠的大脑皮质膜中,与对照品系SAM-R/1相比,加速衰老品系SAM-P/8中[3H]萝芙辛和[3H]尼群地平结合的Bmax值,以及[3H]TCP结合的Kd和Bmax值均显著增加。然而,在海马体膜中,与SAM-R/1相比,SAM-P/8中[3H]奎宁环基苯甲酸酯和[3H]尼群地平结合的Bmax值显著降低。这些结果表明,9个月大的SAM-P/8小鼠的大脑皮质和海马体中,毒蕈碱型乙酰胆碱受体、α2-肾上腺素能受体、N-甲基-D-天冬氨酸受体通道和L型Ca2+通道发生了变化。