Neuroscience 2004 Abstract
| Presentation Number: | 39.1 |
|---|---|
| Abstract Title: | Antagonizing BDNF alters the growth capabilities of injured sensory neurons and signaling pathways. |
| Authors: |
Geremia, N. M.*1
; Pettersson, L. M. E.2
; Hryciw, T.1
; Schreyer, D. J.1
; Danielsen, N.2
; Verge, V. M. K.1
1Cameco MS Neurosci Res Ctr, Saskatoon City Hosp, Saskatoon, Canada 2Sweden, 701 Queen St Rm 5800, S7K OM7, |
| Primary Theme and Topics |
Development - Trophic Factors and Developmental Cell Death -- Neurotrophins: expression and biological effects |
| Secondary Theme and Topics | Development<br />- Trophic Factors and Developmental Cell Death<br />-- Neurotrophins: receptors and signaling mechanisms |
| Session: |
39. Neurotrophins and Receptors I Poster |
| Presentation Time: | Saturday, October 23, 2004 1:00 PM-2:00 PM |
| Location: | San Diego Convention Center - Hall A-H, Board # E23 |
| Keywords: | dorsal root ganglia, nerve injury, neurotrophin, neurite outgrowth |
BDNF is upregulated in injured DRG neurons suggesting a role for this neurotrophin in their regeneration. We reported previously that antagonizing endogenous BDNF results in reduced expression of injury/regeneration-associated genes believed to underly the high capacity for regeneration in these neurons (Geremia et al., 2003 SfN Abstr 38.4). The present study investigates the role of BDNF in modulating neurite outgrowth of injured sensory neurons and the possible intracellular signaling pathways it might regulate as part of the regenerative response. Male Wistar rats underwent unilateral L4,5,6 spinal nerve lesions with anti-BDNF delivered intrathecally for the duration of the 3d injury. Control antibody (Sheep IgG) infusion or spinal nerve injury alone served as controls. L4,5 DRG were removed and cultured in serum free media for 24hrs on laminin and poly-L-lysine coated plates. Injury alone resulted in the highest degree of neurite outgrowth when compared to uninjured neurons. Anti-BDNF infusion resulted in a reduced growth of neurites when compared to controls, but with a minor population of neurons displaying high levels of outgrowth. Other lumbar DRG were processed for immunohistochemistry to detect the levels of phosphorylated (activated) STAT3 or ERK/MAPK. After injury neuronal levels of pERK/MAPK are diminished, but levels are elevated in nonneuronal cells, while pSTAT3 levels are upregulated in injured neurons. Treatment with anti-BDNF results in reduced pERK/MAPK, most evident in nonneuronal cells, with no apparent change in pSTAT3 levels. This preliminary data suggests that endogenous BDNF regulates the ability of injured neurons to grow, likely through an ERK/MAPK pathway.
Supported by CIHR#TOP37537, #ROP102801 & Swedish Research Council 12712.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2004 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2004. Online.
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