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Open Access Highly Accessed Research article

Schwann cells migrate along axons in the absence of GDNF signaling

Stephan Heermann125*, Björn Spittau2, Katalin Zajzon2, Markus H Schwab3 and Kerstin Krieglstein24

Author Affiliations

1 Department of Neuroanatomy, University of Heidelberg, Heidelberg, Germany

2 Department of Molecular Embryology Institute of Anatomy and Cell Biology, University of Freiburg, Freiburg, Germany

3 Department of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany

4 FRIAS, University of Freiburg, Freiburg, Germany

5 Current address: COS Heidelberg, INF, 230 69120, Heidelberg, Germany

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BMC Neuroscience 2012, 13:92  doi:10.1186/1471-2202-13-92

Published: 3 August 2012

Abstract

Background

During development neural crest derived Schwann Cell (SC) precursors migrate to nerve trunks and populate nascent nerves. Axonal ensheathment by SC is a prerequisite for normal nerve function and the integrity of myelinated as well as nonmyelinated axons. To provide adequate support functions, SC colonize entire nerves. One important prerequisite for this is their migration into distal axonal regions.

Results

Here, we studied the role of Glial cell line derived neurotrophic factor (GDNF), a TGF-beta related growth factor, for SC migration. To this end we used a superior cervical ganglion (SCG) explant-SC migration assay, GDNF null mutant mouse embryos and a chemical inhibitor for GDNF signaling in combination with time-lapse imaging. We found that GDNF signaling is dispensable for SC migration along murine embryonic sympathetic axons. Furthermore, in vivo analyzes revealed that SC migration along the sciatic nerve is also not dependent on GDNF.

Conclusions

In contrast to previous in vitro findings in the sciatic nerve and a SC precursor cell line, our results clearly indicate that GDNF is dispensable for embryonic SC migration. This is demonstrated for the sympathetic nervous system and also for the sciatic nerve in mouse.

Keywords:
Schwann cell development; Migration; Proliferation; GDNF; PP2