Ikeda M, Dewar D, McCulloch J
Wellcome Surgical Institute, University of Glasgow, U.K.
Brain Res. 1991 Dec 13;567(1):51-6. doi: 10.1016/0006-8993(91)91434-3.
[125I]Apamin binding sites were examined using quantitative autoradiography in the hippocampus of 9 patients with Alzheimer's disease and 8 age-matched controls. Within the hippocampal formation from control subjects, [125I]apamin binding sites were highly concentrated in the subiculum and CA1. In Alzheimer's disease there was a marked and discrete loss of [125I]apamin binding sites in the subiculum (control = 1.10 +/- 0.10 pmol/g; Alzheimer = 0.71 +/- 0.09 pmol/g) and CA1 (control = 1.41 +/- 0.09 pmol/g; Alzheimer = 0.85 +/- 0.11 pmol/g; values are mean +/- S.E.M.). This reduction of [125I]apamin binding sites in the subiculum correlated with cell density but not neuritic plaque density. These results indicate that an anatomically discrete loss of Ca(2+)-dependent K+ channels within the hippocampal formation occurs in Alzheimer's disease.
使用定量放射自显影技术，在9例阿尔茨海默病患者及8例年龄匹配的对照者的海马中检测了[125I]蜂毒明肽结合位点。在对照者的海马结构中，[125I]蜂毒明肽结合位点高度集中于下托和CA1区。在阿尔茨海默病患者中，下托（对照者=1.10±0.10 pmol/g；阿尔茨海默病患者=0.71±0.09 pmol/g）和CA1区（对照者=1.41±0.09 pmol/g；阿尔茨海默病患者=0.85±0.11 pmol/g；数值为平均值±标准误）的[125I]蜂毒明肽结合位点出现明显且离散性的丧失。下托中[125I]蜂毒明肽结合位点的这种减少与细胞密度相关，但与神经炎性斑块密度无关。这些结果表明，在阿尔茨海默病中，海马结构内存在解剖学上离散的钙依赖性钾通道丧失。
