Meyer M R, Bittner G D
Brain Res. 1978 Mar 24;143(2):213-32. doi: 10.1016/0006-8993(78)90565-6.
Data from previous histological studies indicate that long-term survival of crayfish medial giant axons might be due in part to trophic support from cells of the surrounding glial sheath which often hypertrophy in response to transection of the medial giants. The biochemical studies reported herein show that segments from transected ventral nerve cords (VNC) always incorporate more [3H]leucine into protein than do corresponding segments from intact VNCs. Furthermore, the relative amount of [3H]leucine incorporation in severed segments seems to be influenced by distance and direction from the lesion site as well as time after lesioning. Similar spatiotemporal parameters were previously shown to be correlated with extent of glial hypertrophy around severed medial giant axons. Quantitative autoradiography of medial giant axons after incubation in [3H]leucine revealed that the grain density of label in glial sheaths surrounding severed medial giants was over two-fold greater than in sheaths around corresponding control axons. Moreover, the grain density in the axoplasm of severed medial giants was nearly four-fold greater than the grain density in the axoplasm of control axons. Data from experiments using short or long labeling intervals suggests that labeling in the medial giant axoplasm may be due more to transfer from glial sheath cells than from inherent axonal synthetic mechanisms. In light of this and other data, we concluded that long-term survival of severed medial giant axons is probably due to the direct transfer of trophic substances from cells of the glial sheath into the axon.
以往组织学研究的数据表明,小龙虾内侧巨轴突的长期存活可能部分归因于周围神经胶质鞘细胞的营养支持,这些细胞常因内侧巨轴突横断而肥大。本文报道的生化研究表明,横断腹神经索(VNC)的节段比完整VNC的相应节段总是能将更多的[3H]亮氨酸掺入蛋白质中。此外,切断节段中[3H]亮氨酸掺入的相对量似乎受距损伤部位的距离和方向以及损伤后时间的影响。此前已表明,类似的时空参数与切断的内侧巨轴突周围神经胶质肥大的程度相关。在内侧巨轴突于[3H]亮氨酸中孵育后进行的定量放射自显影显示,切断的内侧巨轴突周围神经胶质鞘中的标记颗粒密度比相应对照轴突周围鞘中的颗粒密度高出两倍多。此外,切断的内侧巨轴突轴浆中的颗粒密度几乎是对照轴突轴浆中颗粒密度的四倍。使用短或长标记间隔的实验数据表明,内侧巨轴突轴浆中的标记可能更多是由于从神经胶质鞘细胞转移而来,而非源于轴突固有的合成机制。鉴于此及其他数据,我们得出结论,切断的内侧巨轴突的长期存活可能是由于营养物质从神经胶质鞘细胞直接转移至轴突。