Axonal regeneration and lack of astrocytic gliosis in EphA4-deficient mice

Goldshmit, Y., Galea, M. P., Wise, G., Bartlett, P. F. and Turnley, A. M. (2004) Axonal regeneration and lack of astrocytic gliosis in EphA4-deficient mice. Journal of Neuroscience, 24 45: 10064-10073. doi:10.1523/JNEUROSCI.2981-04.2004

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Author Goldshmit, Y.
Galea, M. P.
Wise, G.
Bartlett, P. F.
Turnley, A. M.
Title Axonal regeneration and lack of astrocytic gliosis in EphA4-deficient mice
Journal name Journal of Neuroscience   Check publisher's open access policy
ISSN 0270-6474
Publication date 2004-01-01
Sub-type Article (original research)
DOI 10.1523/JNEUROSCI.2981-04.2004
Open Access Status File (Publisher version)
Volume 24
Issue 45
Start page 10064
End page 10073
Total pages 10
Editor Gary L. Westbrook
Place of publication Washington D.C
Publisher Society for Neuroscience
Language eng
Subject C1
320702 Central Nervous System
730104 Nervous system and disorders
Abstract Spinal cord injury usually results in permanent paralysis because of lack of regrowth of damaged neurons. Here we demonstrate that adult mice lacking EphA4 (-/-), a molecule essential for correct guidance of spinal cord axons during development, exhibit axonal regeneration and functional recovery after spinal cord hemisection. Anterograde and retrograde tracing showed that axons from multiple pathways, including corticospinal and rubrospinal tracts, crossed the lesion site. EphA4 -/- mice recovered stride length, the ability to walk on and climb a grid, and the ability to grasp with the affected hindpaw within 1-3 months of injury. EphA4 expression was upregulated on astrocytes at the lesion site in wild-type mice, whereas astrocytic gliosis and the glial scar were greatly reduced in lesioned EphA4-/- spinal cords. EphA4 -/- astrocytes failed to respond to the inflammatory cytokines, interferon-gamma or leukemia inhibitory factor, in vitro. Neurons grown on wild-type astrocytes extended shorter neurites than on EphA4 -/- astrocytes, but longer neurites when the astrocyte EphA4 was blocked by monomeric EphrinA5-Fc. Thus, EphA4 regulates two important features of spinal cord injury, axonal inhibition, and astrocytic gliosis.
Keyword Neurosciences
Spinal Cord Injury
Astrocytic Gliosis
Neurite Outgrowth
Myelin-associated Glycoprotein
Neurite Growth-inhibitors
Reactive Astrocytes
Corticospinal Tract
Nogo-66 Receptor
Tyrosine Kinase
Deficient Mice
Q-Index Code C1

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Created: Wed, 15 Aug 2007, 15:12:41 EST