Holemans S, Javoy-Agid F, Agid Y, De Paermentier F, Laterre E C, Maloteaux J M
Laboratoire de Neurochimie (C 1352), Université Catholique de Louvain, Brussels, Belgium.
Brain Res. 1994 Apr 11;642(1-2):327-33. doi: 10.1016/0006-8993(94)90938-5.
In human brain, [3H]glibenclamide binds with high affinity (KD about 3.5 nM) to sulfonylurea binding sites which are associated with ATP-sensitive potassium (KATP) channels. Regarding to the important neuromodulatory action of KATP channels in some neuronal populations, sulfonylurea binding sites were measured in several cortical areas (frontal and temporal cortex, hippocampus) and striatum (caudate nucleus and putamen) in controls and patients with Parkinson's disease or progressive supranuclear palsy. There was no modification of [3H]glibenclamide specific binding in the cerebral regions studied in both pathologies. These results indicate that KATP channels do not seem to be involved in the pathophysiology of these degenerative processes. Brain samples from five patients with Huntington's disease were studied. A small decrease in sulfonylurea binding sites was measured in the frontal cortex, caudate nucleus and putamen which could be due to the loss of either neurons or nerve endings. This low decrease contrasts with the dramatic diminution of many other markers associated with the profound striatal degeneration occurring in Huntington's disease.
在人脑中，[3H]格列本脲以高亲和力（解离常数KD约为3.5 nM）与磺脲类结合位点结合，这些位点与ATP敏感性钾（KATP）通道相关。鉴于KATP通道在某些神经元群体中具有重要的神经调节作用，在对照组以及帕金森病或进行性核上性麻痹患者的多个皮质区域（额叶和颞叶皮质、海马体）和纹状体（尾状核和壳核）中测量了磺脲类结合位点。在这两种疾病所研究的脑区中，[3H]格列本脲的特异性结合没有改变。这些结果表明，KATP通道似乎不参与这些退行性过程的病理生理。研究了5例亨廷顿病患者的脑样本。在额叶皮质、尾状核和壳核中测量到磺脲类结合位点略有下降，这可能是由于神经元或神经末梢的丢失。这种轻微下降与亨廷顿病中发生的纹状体严重变性相关的许多其他标志物的显著减少形成对比。
