Alund M, Olson L
Brain Res. 1979 Apr 20;166(1):121-37. doi: 10.1016/0006-8993(79)90654-1.
Quinacrine, a fluorescent antimalarial acridine derivative, selectively binds to a population of nerve cell bodies and nerve fibers in Auerbach's plexus and elsewhere in the gut. This quinacrine-binding, as measured by fluorescence intensity, is reduced if the nervous elements are depolarized by high K+ (80--150 MM) or veratridine (5 x 10(-5) M) during quinacrine incubation. A reduction of quinacrine-content in nerve terminals is also seen when depolarization (veratridine) takes place for 2 min after quinacrine-incubation, indicating a release of already bound quinacrine. If terminals are depolarized (high K+ or veratridine) before quinacrine incubation, a reduction of quinacrine content is also seen. The depolarization-induced reduction of quinacrine-binding is blocked by Ca2+-removal and, in the case of veratridine by tetrodotoxin. Our findings suggest that quinacrine binds to a compound that is released by nervous activity. Binding mechanism remains to be elucidated. The possibility that quinacrine visualized purine-rich structures is discussed.
喹吖因,一种荧光抗疟吖啶衍生物,可选择性地与奥尔巴赫神经丛及肠道其他部位的一群神经细胞体和神经纤维结合。在喹吖因孵育期间,如果神经元件被高钾(80 - 150 mM)或藜芦碱(5×10⁻⁵ M)去极化,通过荧光强度测量的这种喹吖因结合会降低。当在喹吖因孵育后进行2分钟的去极化(藜芦碱)时,也可观察到神经末梢中喹吖因含量的减少,这表明已结合的喹吖因被释放。如果在喹吖因孵育前使末梢去极化(高钾或藜芦碱),也会观察到喹吖因含量的减少。去极化诱导的喹吖因结合减少可被去除钙离子所阻断,对于藜芦碱的情况,可被河豚毒素阻断。我们的研究结果表明,喹吖因与神经活动释放的一种化合物结合。结合机制仍有待阐明。文中讨论了喹吖因使富含嘌呤的结构可视化的可能性。