Neuroscience 2001 Abstract
| Presentation Number: | 798.1 |
|---|---|
| Abstract Title: | fibroblast growth factors are involved in retinal ganglion cell axon guidance. |
| Authors: |
Webber, C. A.*1
; McFarlane, S.1
1Genes and Development Research Group, University of Calgary, Calgary, Canada |
| Primary Theme and Topics |
Development - Axonal and Dendritic Development -- Axon outgrowth: receptors and signaling mechanisms |
| Session: |
798. Axonal and dendritic development: axon growth and guidance--growth factors, trophic factors Poster |
| Presentation Time: | Wednesday, November 14, 2001 1:00 PM-2:00 PM |
| Location: | Exhibit Hall C-2 |
| Keywords: | growth cone, <i>Xenopus</i>, retinotectal, axon extension |
Evidence suggests that fibroblast growth factors (FGFs) stimulate axon extension of Xenopus retinal ganglion cell (RGC) neurons. Growth cones express the FGF receptor (FGFR); cells along the optic pathway express FGF-2; FGF-2 promotes axon extension in vitro, and; misexpression of a dominant negative FGFR decreases neurite extension both in vivo and in vitro. The present study aims to determine if FGFs simply promote axon extension or if they chemotropically direct RGC axon trajectories.
Thus, we asked if FGF expression alongside the extending optic projection misdirects RGC axons. To determine this, we cotransfected plasmids containing the green fluorescent protein (GFP) and embryonic FGF (eFGF) cDNAs into the neuroepithelium of stage 24 Xenopus embryos. At stage 40, when RGC axons normally have reached the optic tectum, we labeled the axons with horse radish peroxidase (HRP). HRP labeled RGC axons that contact GFP misexpressing neurons along the optic pathway project normally to the tectum. In contrast, RGC axons avoid GFP/eFGF misexpressing cells.
To better understand why RGC axons are repulsed by eFGF positive cells, we examined if: 1) eFGF positive cells are undifferentiated. BrdU labeling suggests the cells are post-mitotic. 2) if FGF misexpression causes upregulation of inhibitory guidance molecules. Ephrin B1 (a guidance molecule known to be inhibitory to RGC axons) is not upregulated 3) if FGF is inhibitory at high concentrations. Ten times higher FGF-2 levels in culture than is normally needed to promote axon extension is still stimulatory to RGC axon outgrowth.
Our data support the idea that FGFs may act as guidance molecules for RGC axons.
Thus, we asked if FGF expression alongside the extending optic projection misdirects RGC axons. To determine this, we cotransfected plasmids containing the green fluorescent protein (GFP) and embryonic FGF (eFGF) cDNAs into the neuroepithelium of stage 24 Xenopus embryos. At stage 40, when RGC axons normally have reached the optic tectum, we labeled the axons with horse radish peroxidase (HRP). HRP labeled RGC axons that contact GFP misexpressing neurons along the optic pathway project normally to the tectum. In contrast, RGC axons avoid GFP/eFGF misexpressing cells.
To better understand why RGC axons are repulsed by eFGF positive cells, we examined if: 1) eFGF positive cells are undifferentiated. BrdU labeling suggests the cells are post-mitotic. 2) if FGF misexpression causes upregulation of inhibitory guidance molecules. Ephrin B1 (a guidance molecule known to be inhibitory to RGC axons) is not upregulated 3) if FGF is inhibitory at high concentrations. Ten times higher FGF-2 levels in culture than is normally needed to promote axon extension is still stimulatory to RGC axon outgrowth.
Our data support the idea that FGFs may act as guidance molecules for RGC axons.
Supported by CIHR and AHFMR
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2001 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2001. Online.
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