Aletta J M, Goldberg D J
J Neurosci. 1984 Jul;4(7):1800-8. doi: 10.1523/JNEUROSCI.04-07-01800.1984.
The regulation of the quantities and types of organelles that leave the neuronal cell body destined for use in the axon and its terminals is not well understood. We had previously found that transport of transmitter undergoes a precise down regulation when most of one branch of the bifurcate axon of an identified serotonergic neuron was removed. We have now investigated further the nature of the regulatory event and the reason for its initiation by eliminating portions of the axonal tree of this neuron. We find that the down regulation is more likely to be due to the loss of synapses than of axon because transport of [3H]serotonin decreases as much when an axonal branch is transected distally as after a proximal transection. Transport of [3H]fucosyl glycoprotein, which normally is associated with the serotonergic vesicle in this axon, decreases to the same extent as transport of [3H]serotonin following proximal transection. The glycoprotein down regulation occurs much more rapidly, possibly due to an inhibition of vesicle synthesis. A secondary rise in transport of [3H] fucosyl glycoprotein 3 days to 2 weeks after axotomy suggests that the radiolabeled glycoprotein has undergone a redistribution into organelles not normally labeled and transported in intact neurons in large amounts, since [3H]serotonin transport remains stably diminished during this period. We also describe here a case of routing of rapidly transported material. When one axonal branch is cut far from the point of bifurcation (approximately 10 mm), [3H]serotonin is directed away from the ranch lacking its synaptic terminals and into the remaining intact branch even though the transected branch is physically capable of transporting its normal amount of [3H]serotonin.(ABSTRACT TRUNCATED AT 250 WORDS)
对于离开神经元细胞体、用于轴突及其终末的细胞器的数量和类型的调控,目前还了解得不够充分。我们之前发现,当一个已鉴定的5-羟色胺能神经元的二叉状轴突的一个分支的大部分被切除时,递质的运输会经历精确的下调。我们现在通过切除该神经元轴突树的部分区域,进一步研究了这种调控事件的本质及其启动原因。我们发现,下调更可能是由于突触的丧失而非轴突的丧失,因为当轴突分支在远端横断时,[3H]5-羟色胺的运输减少程度与近端横断后相同。[3H]岩藻糖基糖蛋白的运输,正常情况下与该轴突中的5-羟色胺能囊泡相关,在近端横断后,其减少程度与[3H]5-羟色胺的运输相同。糖蛋白的下调发生得更快,可能是由于囊泡合成受到抑制。轴突切断后3天至2周,[3H]岩藻糖基糖蛋白运输的二次上升表明,放射性标记的糖蛋白已重新分布到完整神经元中通常不会大量标记和运输的细胞器中,因为在此期间[3H]5-羟色胺的运输仍稳定减少。我们在此还描述了一个快速运输物质的路由情况。当一个轴突分支在远离分叉点(约10毫米)处被切断时,[3H]5-羟色胺会被导向缺乏突触终末的分支之外,进入剩余的完整分支,即使被横断的分支在物理上能够运输其正常量的[3H]5-羟色胺。(摘要截短于250字)