Journal
JOURNAL OF NEUROSCIENCE
Volume 27, Issue 9, Pages 2176-2185Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.5176-06.2007
Keywords
chondroitin sulfate; axon regeneration; spinal cord injury; traumatic injury; dorsal rhizotomy; proteoglycan
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Funding
- NINDS NIH HHS [R37 NS033020-17, R01 NS039962, R01 NS039962-10, R37 NS033020] Funding Source: Medline
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Axotomized neurons within the damaged CNS are thought to be prevented from functional regeneration by inhibitory molecules such as chondroitin sulfate proteoglycans (CSPGs) and myelin-associated inhibitors. Here, we provide a transgenic test of the role of CSPGs in limiting regeneration, using the gfap promotor to express a CSPG-degrading enzyme chondroitinase ABC (ChABC) in astrocytes. Corticospinal axons extend within the lesion site, but not caudal to it, after dorsal hemisection in the transgenic mice. The presence of the gfap-ChABC transgene yields no significant improvement in motor function recovery in this model. In contrast, functionally significant sensory axon regeneration is observed after dorsal rhizotomy in transgenic mice. These transgenic studies confirm a local efficacy for reduced CSPG to enhance CNS axon growth after traumatic injury. CSPGs appear to function in a spatially distinct role from myelin inhibitors, implying that combination-based therapy will be especially advantageous for CNS injuries.
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