Chang A C, Dellmann H D
Exp Brain Res. 1984;53(2):357-69. doi: 10.1007/BF00238166.
The microiontophoretic ejection of vinblastine into the median eminence effectively blocked axonal transport in the hypothalamoneurohypophysial system of the frog. Proximal to the ejection site, large axon swellings (Herring bodies) were found that contained mainly abundant neurosecretory granulated vesicles and axonal smooth endoplasmic reticulum. At advanced post ejection times, autophagic events were obvious. Subsequently, preexperimental conditions were reestablished, indicative of the resumption of axonal transport. Distal to the ejection site, i.e. in the neural lobe, the relatively long block of axonal transport subsequent to the vinblastine ejection caused most axons to degenerate and to be phagocytized by pituicytes. The degenerative process was reversible since upon reestablishment of the axonal transport regeneration of the neurosecretory fibers occurred.
将长春碱微量离子电渗注入到蛙正中隆起中,可有效阻断蛙下丘脑 - 神经垂体系统中的轴突运输。在注入部位近端,发现有大的轴突肿胀(赫林体),其主要含有丰富的神经分泌颗粒小泡和轴突滑面内质网。在注入后晚期,自噬事件明显。随后,恢复到实验前状态,这表明轴突运输已恢复。在注入部位远端,即在神经叶,长春碱注入后轴突运输的相对长时间阻断导致大多数轴突退化并被垂体细胞吞噬。由于轴突运输恢复后神经分泌纤维发生再生,因此退化过程是可逆的。