Ruberg M, Mayo W, Brice A, Duyckaerts C, Hauw J J, Simon H, LeMoal M, Agid Y
INSERM U. 289, Hôpital de la Salpêtrière, Paris, France.
Neuroscience. 1990;35(2):327-33. doi: 10.1016/0306-4522(90)90086-j.
[3H]Vesamicol binding was characterized in human brain post mortem. The number of binding sites was then determined in parallel with choline acetyltransferase activity in the temporal cortex of patients with Alzheimer's disease, demented and non-demented patients with Parkinson's disease, and in the cerebral cortex of rats with quisqualic acid lesions of the nucleus basalis magnocellularis. Whereas choline acetyltransferase activity decreased in patients with Alzheimer's or Parkinson's disease indicating loss of cholinergic innervation, the number of binding sites for [3H]vesamicol was the same as or higher than in controls. Similar results were obtained with the lesioned rats. It is suggested that the increase in binding sites may reflect compensatory regulation of the spared neurons at the level of the synaptic vesicle.
用[3H]维生霉素结合法对人脑进行尸检研究。随后，在患有阿尔茨海默病的患者、患有帕金森病的痴呆和非痴呆患者的颞叶皮质，以及在巨细胞基底核注射喹啉酸损伤的大鼠大脑皮质中，并行测定结合位点数量与胆碱乙酰转移酶活性。阿尔茨海默病或帕金森病患者的胆碱乙酰转移酶活性降低，表明胆碱能神经支配丧失，而[3H]维生霉素的结合位点数量与对照组相同或更高。损伤大鼠也得到了类似结果。提示结合位点增加可能反映了突触小泡水平上备用神经元的代偿性调节。
