Abstract
<h4>Background and purpose</h4>Improvement in axonal regeneration may lead to the
development of longer nerve grafts and improved outcomes for patients with peripheral
nerve injury. Although the use of acellular nerve grafts has been well documented
(Groves et al, Exp Neurol. 2005;195:278-292; Krekoski et al, J Neurosci. 2001;21:6206-6213;
Massey et al, Exp Neurol. 2008;209:426-445; Neubauer et al, Exp Neurol. 2007;207:163-170;
Zuo et al, Exp Neurol. 2002;176:221-228), less is known about the ability of neurotrophic
factors to enhance axonal regeneration. This study evaluates axonal ingrowth augmentation
using acellular, chondroitinase-treated nerve grafts doped with nerve growth factor
(NGF).<h4>Methods</h4>Acellular chondroitinase-treated murine nerve grafts were placed
in experimental (NGF-treated grafts) and control (carrier-only grafts) rats. Five
days after implantation, axonal regeneration was assessed by immunocytochemistry along
with digital image analysis.<h4>Results</h4>Higher axon count was observed throughout
the length of the nerve in the NGF group (P < 0.0001), peaking at 3 mm from proximal
repair (P = 0.02). Although the NGF group displayed a higher axon count per slice,
the mean diameter of individual NGF axons was smaller (P < 0.0001), potentially consistent
with induction of sensory axons (Rich et al, J Neurocytol. 1987;16:261-268; Sofroniew
et al, Annu Rev Neurosci. 2001;24:1217-1128; Yip et al, J Neurosci. 1984;4:2986-2992).<h4>Conclusion</h4>The
simple technique of doping acellular, chondroitinase-treated nerve grafts with NGF
can augment axonal ingrowth and possibly preferentially induce sensory axons.
Published Version (Please cite this version)
10.1097/sap.0b013e3182380974
Material is made available in this collection at the direction of authors according
to their understanding of their rights in that material. You may download and use
these materials in any manner not prohibited by copyright or other applicable law.
Rights for Collection: Research and Writings
Works are deposited here by their authors, and
represent their research and opinions, not that of Duke University. Some materials
and descriptions may include offensive content.
More info