Qiao Li-Ya, Vizzard Margaret A
Department of Neurology, University of Vermont College of Medicine, Burlington, Vermont 05405, USA.
J Comp Neurol. 2005 Feb 7;482(2):142-54. doi: 10.1002/cne.20394.
Previous studies have demonstrated increased expression and phosphorylation of tyrosine kinase receptor (TrkA, TrkB) in lumbosacral DRG after chronic (6 weeks) spinal cord (T8-T10) injury. This study examined the effects of acute SCI (48 hours, 2 weeks) on TrkA and TrkB expression and phosphorylation, and CREB and c-Jun expression in DRG. A significant increase in the number of TrkA- (1.5-3-fold; P < or = 0.05), TrkB- (1.3-2.0-fold; P < or = 0.05), and phosphorylated Trk (pTrk)-immunoreactive (1.5-3-fold; P < or = 0.05) cells was observed in the L1, L6, and S1 DRG 48 hours, 2, or 6 weeks after SCI. A significant increase in the number of phosphorylated (p-) CREB-immunoreactive cells was observed in the L1, L2, L6, and S1 DRG 48 hours, 2, or 6 weeks after SCI. The largest changes in p-CREB-immunoreactivity were in L1 and L2 DRG (10-fold; P <or= 0.01) at 48 hours after SCI; however, changes were modest in bladder afferent neurons. After SCI, the overall number of c-Jun-immunoreactive cells in L1, L2, and S1 DRG was dramatically increased (3-10-fold; P < or = 0.01); however, only a low percentage of bladder afferent cells expressed c-Jun-IR before or after SCI. In summary, these results suggest that TrkA or TrkB may be involved in reorganization of micturition pathways after SCI. However, CREB or c-Jun may not be downstream transcription factors in Trk-mediated signaling cascades in micturition reflex pathways after SCI but may play a role in other, nonbladder SCI-induced changes.
先前的研究表明，在慢性（6周）脊髓（T8 - T10）损伤后，腰骶部背根神经节（DRG）中酪氨酸激酶受体（TrkA、TrkB）的表达和磷酸化增加。本研究检测了急性脊髓损伤（48小时、2周）对DRG中TrkA和TrkB表达及磷酸化，以及CREB和c - Jun表达的影响。在脊髓损伤后48小时、2周或6周时，在L1、L6和S1 DRG中观察到TrkA免疫反应性细胞数量显著增加（1.5至3倍；P≤0.05）、TrkB免疫反应性细胞数量显著增加（1.3至2.0倍；P≤0.05）以及磷酸化Trk（pTrk）免疫反应性细胞数量显著增加（1.5至3倍；P≤0.05）。在脊髓损伤后48小时、2周或6周时，在L1、L2、L6和S1 DRG中观察到磷酸化（p -）CREB免疫反应性细胞数量显著增加。p - CREB免疫反应性变化最大的是在脊髓损伤后48小时的L1和L2 DRG（10倍；P≤0.01）；然而，膀胱传入神经元中的变化较小。脊髓损伤后，L1、L2和S1 DRG中c - Jun免疫反应性细胞的总数显著增加（3至10倍；P≤0.01）；然而，在脊髓损伤前后，只有低比例的膀胱传入细胞表达c - Jun免疫反应性。总之，这些结果表明TrkA或TrkB可能参与脊髓损伤后排尿通路的重组。然而，CREB或c - Jun可能不是脊髓损伤后排尿反射通路中Trk介导的信号级联反应的下游转录因子，但可能在其他非膀胱脊髓损伤诱导的变化中起作用。
