Shadiack A M, Vaccariello S A, Sun Y, Zigmond R E
Department of Neurosciences, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106-4975, USA.
Proc Natl Acad Sci U S A. 1998 Jun 23;95(13):7727-30. doi: 10.1073/pnas.95.13.7727.
Axonal damage to adult peripheral neurons causes changes in neuronal gene expression. For example, axotomized sympathetic, sensory, and motor neurons begin to express galanin mRNA and protein, and recent evidence suggests that galanin plays a role in peripheral nerve regeneration. Previous studies in sympathetic and sensory neurons have established that galanin expression is triggered by two consequences of nerve transection: the induction of leukemia inhibitory factor (LIF) and the reduction in the availability of the target-derived factor, nerve growth factor. It is shown in the present study that no stimulation of galanin expression occurs following direct application of LIF to intact neurons in the superior cervical sympathetic ganglion. Injection of animals with an antiserum to nerve growth factor concomitant with the application of LIF, on the other hand, does stimulate galanin expression. The data suggest that the response of neurons to an injury factor, LIF, is affected by whether the neurons still receive trophic signals from their targets.
成年外周神经元的轴突损伤会导致神经元基因表达发生变化。例如，轴突被切断的交感神经、感觉神经和运动神经元开始表达甘丙肽mRNA和蛋白质，最近的证据表明甘丙肽在周围神经再生中起作用。先前对交感神经和感觉神经元的研究表明，甘丙肽的表达是由神经横断的两个后果触发的：白血病抑制因子（LIF）的诱导和靶源性因子神经生长因子可用性的降低。本研究表明，将LIF直接应用于颈上交感神经节的完整神经元后，不会刺激甘丙肽的表达。另一方面，在应用LIF的同时给动物注射抗神经生长因子抗血清确实会刺激甘丙肽的表达。数据表明，神经元对损伤因子LIF的反应受神经元是否仍从其靶标接收营养信号的影响。
