Spinal cord injury‐induced expression of TrkA, TrkB, phosphorylated CREB, and c‐Jun in rat lumbosacral dorsal root ganglia
- 20 December 2004
- journal article
- research article
- Published by Wiley in Journal of Comparative Neurology
- Vol. 482 (2), 142-154
- https://doi.org/10.1002/cne.20394
Abstract
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 ≤ 0.05), TrkB- (1.3–2.0-fold; P ≤ 0.05), and phosphorylated Trk (pTrk)-immunoreactive (1.5–3-fold; P ≤ 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 ≤ 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 ≤ 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. J. Comp. Neurol. 482:142–154, 2005.Keywords
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