Gehlert D R, Morey W A, Wamsley J K
J Neurosci Res. 1985;13(3):443-52. doi: 10.1002/jnr.490130310.
Animals fed a diet deficient in thiamine or treated with a drug preventing the utilization of thiamine (thiamine antagonist) exhibited alterations in ligand binding to muscarinic receptors in several brain regions. Using quantitative techniques of receptor autoradiography, an increase in muscarinic receptor binding was demonstrated in such regions as the corpus callosum, lamina VI of the parietal cortex, caudate-putamen, ventral nucleus of the thalamus, stratum lacunosum moleculare and stratum oriens of the hippocampus, and the hilus of the area dentata. As a result of thiamine deficiency, this increase in muscarinic receptor populations was primarily due to an increase in the binding of the low-affinity agonist site. In the same experiment, a decrease in muscarinic receptor binding was found in the ventromedial region of the hypothalamus. Thiamine deficiency thus causes an up-regulation of muscarinic receptor binding in several regions of rat brain while causing a down-regulation of these same receptors in other brain areas.
喂食缺乏硫胺素的饮食或用阻止硫胺素利用的药物(硫胺素拮抗剂)处理的动物,在几个脑区中表现出与毒蕈碱受体的配体结合发生改变。使用受体放射自显影定量技术,在胼胝体、顶叶皮质第VI层、尾状核-壳核、丘脑腹侧核、海马分子层腔隙层和海马原层以及齿状回门等区域证实毒蕈碱受体结合增加。由于硫胺素缺乏,毒蕈碱受体数量的这种增加主要是由于低亲和力激动剂位点的结合增加。在同一实验中,在下丘脑腹内侧区域发现毒蕈碱受体结合减少。因此,硫胺素缺乏导致大鼠脑的几个区域中毒蕈碱受体结合上调,而在其他脑区中导致这些相同受体下调。