Neuroscience 2000 Abstract
| Presentation Number: | 324.2 |
|---|---|
| Abstract Title: | Replacement of GAP-43 and CAP-23 induces spinal cord axon regeneration. |
| Authors: |
Bulsara, K. R.*1
; Bomze, H. M.1
; Skene, J. H. P.1
1Neurobiology, Duke Univ., Durham, NC |
| Primary Theme and Topics |
A. Development and Regeneration - 22. Regeneration |
| Secondary Theme and Topics | A. Development and Regeneration<br />- 6. Process outgrowth, growth cones and sprouting |
| Session: |
324. Regeneration VI Poster |
| Presentation Time: | Monday, November 6, 2000 2:00 PM-3:00 PM |
| Location: | Hall G-J |
| Keywords: | growth-associated proteins, growth cones, CNS regeneration, dorsal root ganglion |
In vivo , peripheral nerve injury enables adult dorsal root ganglion (DRG) neurons to support regeneration of their spinal cord axons (Richardson & Issa, Nature 309:79,1984. It is not known which of the genes induced by this injury are needed for regeneration. In vitro, combined expression of GAP-43 and CAP-23, two prominent growth cone proteins, can mimic peripheral nerve injury in triggering the extension of long axons by adult DRG neurons (Bomze et. al, this volume). To determine whether replacement of these two proteins is sufficient to induce regeneration in vivo, we made bilateral dorsal column lesions that sever the central axons of DRG neurons in wild-type mice and in transgenic animals expressing both GAP-43 and CAP-23. A segment of peripheral nerve (sciatic) was resected on one side and grafted into the lesion site. After 1-4 months, diI was introduced into the distal end of the graft to retrogradely label the cell bodies of those axons that had regenerated into the graft. DRG subjected to the peripheral injury contained numerous labeled neurons (60-70 per ganglion; n=5 animals). Without a peripheral lesion, DRG neurons of non-transgenic mice were unable to extend their spinal axons into the nerve graft (mean of 0.4 labeled per ganglion; n=5 animals). In the transgenic mice, however, combined expression of GAP-43 and CAP-23 induced a 50-fold increase in the number of DRG neurons that can regenerate their spinal axons (23 per ganglion; n=5) without peripheral nerve injury. Thus, sustained expression of GAP-43 and CAP-23 is sufficient to mimic the effects of peripheral injury in activating axon regeneration following spinal cord injury in vivo. Supported by NIH grant EY11475, Novartis, and an R.K. Broad Fellowship.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2000 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2000. Online.
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