Bates D J, Sirkos S, Moses E K, Austin L
Neurochem Res. 1983 Mar;8(3):363-74. doi: 10.1007/BF00965726.
An in vitro procedure for labeling of RNA in the excised rat nodose ganglion was used to evaluate the changes in incorporation of [3H]uridine into ganglionic RNA following transection of the abdominal vagus nerves. Significant increases in the incorporation into 28S, 18S and 4S RNA were observed at 1 day after injury, which were maximal at 4 days before returning to unoperated control level by 7 days. A second transient increase in the labelling of these RNA species occurred between 9 and 11 days after injury. Comparison of the time course of these increases with those seen previously following cervical vagus nerve crush injury indicate that the time of onset of the increase in incorporation in independent of the site of injury, but that the maximal response is delayed by 1 day with the more distal lesion. These data are consistent with the existence of separate signals for initiating and modulating the cell body response to axon injury, which are transported retrogradely from the site of injury at rates exceeding the slow component of axoplasmic transport.
采用一种体外标记大鼠离体结状神经节RNA的方法，来评估切断腹部迷走神经后[3H]尿苷掺入神经节RNA的变化。损伤后1天观察到28S、18S和4S RNA掺入量显著增加，4天时达到最大值，到7天时恢复到未手术对照水平。这些RNA种类标记的第二次短暂增加发生在损伤后9至11天之间。将这些增加的时间进程与先前颈迷走神经挤压伤后的情况进行比较表明，掺入增加的起始时间与损伤部位无关，但更远端损伤的最大反应延迟1天。这些数据与存在分别启动和调节细胞体对轴突损伤反应的信号相一致，这些信号以超过轴浆运输慢成分的速率从损伤部位逆行运输。
