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The Journal of Neuroscience, January 31, 2007, 27(5):1190-1199; doi:10.1523/JNEUROSCI.5089-06.2007

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Development/Plasticity/Repair
Impaired Axonal Regeneration by Isolectin B4-Binding Dorsal Root Ganglion Neurons In Vitro

Pascal G. Leclere,¹ Emma Norman,¹ Filitsa Groutsi,² Robert Coffin,² Ulrike Mayer,³ John Pizzey,¹ and David Tonge¹

¹The Wolfson Centre for Age Related Diseases, School of Biomedical and Health Sciences, King's College London, London SE1 1UL, United Kingdom, ²Department of Immunology and Molecular Pathology, University College London, London W1T 4JF, United Kingdom, and ³Biomedical Research Centre, School of Biological Sciences, University of East Anglia, Norwich NR14 7TJ, United Kingdom

Correspondence should be addressed to Dr. David Tonge, The Wolfson Centre for Age Related Diseases, School of Biomedical and Health Sciences, King's College London, Guy's Campus, London SE1 1UL, UK. Email: david.tonge{at}kcl.ac.uk

The subpopulation of dorsal root ganglion (DRG) neurons recognized by Griffonia simplicifolia isolectin B4 (IB4) differ from other neurons by expressing receptors for glial cell line-derived neurotrophic factor (GDNF) rather than neurotrophins. Additionally, IB4-labeled neurons do not express the laminin receptor, 7-integrin (Gardiner et al., 2005), necessary for optimal axonal regeneration in the peripheral nervous system. In cultures of dissociated DRG neurons of adult mice on laminin, robust spontaneous neurite outgrowth from IB4-negative neurons occurs and is strongly enhanced by previous axotomy. In contrast, IB4-labeled neurons show little neurite outgrowth and do not express GAP 43, even after axotomy or culture with GDNF. Moreover, growth of their axons through collagen gels is impaired compared with other DRG neurons. To determine whether the sparse neurite outgrowth of IB4-labeled neurons is attributable to lack of integrin expression, DRG cultures were infected with a herpes simplex 1 vector encoding 7-integrin, but its forced expression failed to promote neurite outgrowth in either IB4-labeled or other DRG neurons or in cultured adult retinal ganglion cells. Forced coexpression of both 7-integrin and GAP 43 also failed to promote neurite outgrowth in IB4-labeled neurons. In addition, cultured sciatic nerve segments were found to release much lower levels of GDNF, demonstrated by ELISA, than nerve growth factor. These findings together with their impaired intrinsic axonal regeneration capacity may contribute to the known vulnerability of the IB4-labeled population of DRG neurons to peripheral nerve injury.

Key words: DRG; IB4; 7-integrin; GAP 43; SPRR1A; axonal regeneration

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Received Aug. 21, 2006; revised Dec. 14, 2006; accepted Dec. 16, 2006.

Correspondence should be addressed to Dr. David Tonge, The Wolfson Centre for Age Related Diseases, School of Biomedical and Health Sciences, King's College London, Guy's Campus, London SE1 1UL, UK. Email: david.tonge{at}kcl.ac.uk

This article has been cited by other articles:

				D. Wu, W. Huang, P. M. Richardson, J. V. Priestley, and M. Liu TRPC4 in Rat Dorsal Root Ganglion Neurons Is Increased after Nerve Injury and Is Necessary for Neurite Outgrowth J. Biol. Chem., January 4, 2008; 283(1): 416 - 426. [Abstract] [Full Text] [PDF]

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