Effects of systemically administered NT-3 on sensory neuron loss and nestin expression following axotomy
Article first published online: 24 JAN 2005
Copyright © 2005 Wiley-Liss, Inc.
Journal of Comparative Neurology
Volume 482, Issue 4, pages 320–332, 21 February 2005
How to Cite
Kuo, L.-T., Simpson, A., Schänzer, A., Tse, J., An, S.-F., Scaravilli, F. and Groves, M. J. (2005), Effects of systemically administered NT-3 on sensory neuron loss and nestin expression following axotomy. J. Comp. Neurol., 482: 320–332. doi: 10.1002/cne.20400
- Issue published online: 24 JAN 2005
- Article first published online: 24 JAN 2005
- Manuscript Accepted: 29 SEP 2004
- Manuscript Revised: 16 SEP 2004
- Manuscript Received: 18 AUG 2004
- Brain Research Trust (Neurogenesis in adult rat dorsal root ganglia, 2000–2002)
- dorsal root ganglia
Previous work has shown that administration of the neurotrophin NT-3 intrathecally or to the proximal stump can prevent axotomy-induced sensory neuron loss and that NT-3 can stimulate sensory neuron differentiation in vitro. We have examined the effect of axotomy and systemic NT-3 administration on neuronal loss, apoptosis (defined by morphology and activated caspase-3 immunoreactivity), and nestin expression (a protein expressed by neuronal precursor cells) in dorsal root ganglia (DRG) following axotomy of the adult rat sciatic nerve. Systemic administration of 1.25 or 5 mg of NT-3 over 1 month had no effect on the incidence of apoptotic neurons but prevented the overall loss of neurons seen at 4 weeks in vehicle-treated animals. Nestin-immunoreactive neurons began to appear 2 weeks after sciatic transection in untreated animals and steadily increased in incidence over the next 6 weeks. NT-3 administration increased the number of nestin-immunoreactive neurons at 1 month by two- to threefold. Nestin-IR neurons had a mean diameter of 20.78 ± 2.5 μm and expressed the neuronal markers neurofilament 200, βIII-tubulin, protein gene product 9.5, growth associated protein 43, trkA, and calcitonin gene-related peptide. Our results suggest that the presence of nestin in DRG neurons after nerve injury is due to recent differentiation and that exogenous NT-3 may prevent neuron loss by stimulating this process, rather than preventing neuron death. J. Comp. Neurol. 482:320–332, 2005. © 2005 Wiley-Liss, Inc.