Neuroscience 2003 Abstract
| Presentation Number: | 357.10 |
|---|---|
| Abstract Title: | Regulation of the response of injured spindle afferents by muscle-derived neurotrophin-3. |
| Authors: |
Taylor, M. D.*1
; Vorontsova, E.2
; Fowler, S. C.2
; Holdeman, A. S.1
; Ryals, J. M.1
; Wright, D. E.1
1Anat. & Cell. Biol, Univ. Kansas Med. Ctr, Kansas City, KS 2KS, 3901 Rainbow Blvd, 66160, |
| Primary Theme and Topics |
Development - Transplantation and Regeneration -- Regeneration: PNS |
| Secondary Theme and Topics | Development<br />- Trophic Factors and Developmental Cell Death<br />-- Neurotrophins: expression and biological effects |
| Session: |
357. PNS Regeneration: Mechanisms Poster |
| Presentation Time: | Monday, November 10, 2003 9:00 AM-10:00 AM |
| Location: | Morial Convention Center - Hall F-I, Board # C31 |
| Keywords: | PROPRIOCEPTIVE, NERVE INJURY, NT-3, SENSORIMOTOR |
Neurotrophin-3 (NT-3) has been well characterized as a survival factor for large proprioceptive DRG neurons. Postnatally, NT-3 expression in skeletal muscle becomes restricted to muscle spindles and likely continues to support proprioceptive neurons. Transgenic mice overexpressing NT-3 in skeletal muscle under control of the myosin light chain promoter (mlc/NT-3 mice) have been used as a model to investigate the neuroprotective effects of muscle-derived NT-3 following peripheral nerve injury. Studies assessing the consequences of nerve crush on retrograde transport, neuronal survival, axonal morphology, muscle spindle innervation, and locomotor performance all suggest that delayed axonal degeneration of proprioceptive neurons may occur in mice that overexpress NT-3 in muscle following sciatic nerve crush (Taylor et al., 2002 SFN 821.1). Moreover, immunohistochemical analysis of the innervation of entire muscle spindles revealed that injured sensory and motor axons retract from and reinnervate intrafusal fibers in a strict hierarchical fashion that recapitulates the initial innervation of spindles during development. The hypothesis that NT-3 may delay the degeneration of spindle afferents was tested by treating wildtype mice with exogenous NT-3 prior to and following nerve injury. To date, intramuscular injection of low doses of human recombinant NT-3 (1µg) treatment failed to produce similar delays in axonal degeneration following nerve injury. Current studies are underway to test higher doses and longer treatment periods. Finally, force plate actometry was utilized to precisely monitor locomotive parameters of mlc/NT-3 and wildtype littermates following nerve injury. Together, these studies are providing insight into the mechanisms by which muscle-derived NT-3 affects the response to injury of proprioceptive axons.
Supported by R29NS37910 and PO1DE07734
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2003 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2003. Online.
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