Neuroscience 2003 Abstract
| Presentation Number: | 142.11 |
|---|---|
| Abstract Title: | Reduced axon growth in cultured embryonic spinal motoneurons from prnp-/- mice. |
| Authors: |
Wiese, S.*1
; Flechsig, E.2
; Klein, M. A.2
; Sendtner, M.1
1Univ. of Wuerzburg, Inst. Clin. Neurobiol, Wuerzburg, Germany 2Germany, Josef Schneider-Str 11, D-97080, |
| Primary Theme and Topics |
Development - Axonal and Dendritic Development -- Axon growth and guidance: receptors and signaling mechanisms |
| Session: |
142. Axon Growth and Guidance: Receptors and Signaling Mechanisms--Receptors Poster |
| Presentation Time: | Sunday, November 9, 2003 10:00 AM-11:00 AM |
| Location: | Morial Convention Center - Hall F-I, Board # B33 |
| Keywords: | spongiforme enzephalitis, prion, survival, axon |
The cellular prion protein (PrPC) plays a crucial role in transmissible spongiform encephalopathies (TSEs). PrPC and is predominanatly expressed in brain, at neuronal synapses, axons and cell bodies. It is attached by a glycosyl-phosphatidyl inositol (GPI) anchor to the outer cell surface and its physiological function is still elusive. PrP knockout mice (prnp-/-), in which only the PrP coding sequence was disrupted, develop normally and remain healthy after birth. Several lines of evidence suggest a role of PrPC in neurite outgrowth. We have investigated the effect of PrPC expression on survival and axon growth using motoneurons from prnp-/-, prnp+/- and wild-type mice. These motoneurons were cultured with BDNF, CNTF or GDNF as a neurotrophic factor. No reduction in cell survival was observed but axon length was significantly shorter in comparison to heterozygote or wild-type controls. The reduction of axon length occured independently of the neurotrophic factor applied, and with both laminin or laminin-2 (merosin) as a substrate. PrP protein was localised on axons and cell bodies of cultured motoneurons. We also performed motoneuron cultures from prnp-/-/ PRPTG20A mice which overexpress PrP as a transgene on the prnp-/- background. With this PrP transgene overexpression the axonal defect observed in the prnp-/- motoneurons appeared rescued. These results indicate that PrPC expression on cultured motoneurons is not necessary for cell survival but axonal growth and maintenance.
Supported by Bayr. Prionenforscherverbund
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2003 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2003. Online.
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