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Neuroscience 2004 Abstract

Presentation Number: 298.10
Abstract Title: Pharmacological assessment of chronic pain in a rat bone fracture model.
Authors: Roudier, M. P.*1 ; Brot, M. D.1 ; Lin, C.1 ; Haynes, K. S.1 ; Wiley, J. S.1 ; Panzitta, T.1 ; Feldman, R. S.1 ; Campbell, M.1 ; Bain, S. D.1
1SkeleTech, Bothell, WA

Primary Theme and Topics Sensory Systems
- Pain
-- Spinal cord processing: anatomy and physiology
Secondary Theme and Topics Techniques in Neuroscience<br />- Staining, tracing and imaging techniques
Session: 298. Pain Models
Poster
Presentation Time: Sunday, October 24, 2004 2:00 PM-3:00 PM
Location: San Diego Convention Center - Hall A-H, Board # R11
Keywords: Pain, Spinal cord, Allodynia, Bone
Chronic bone pain in osteoporosis is a commonly encountered clinical problem. Previously, we have shown that a closed femur fracture model in the rat can be used to model the enduring pain that follows bone fracture (Brot et al, SFN 2003). In order to further characterize the hyperalgesia observed in this model we have investigated commonly used pain medications for their effects on mechanical hyperalgesia and spinal GFAP staining . Male Sprague-Dawley rats received either a sham surgery or a right femur closed fracture with intramedullary pin (CF+PIN) or a pin insertion (PIN) only. Three weeks after surgery, the rats were tested for mechanical hyperalgesia using the von Frey technique. In addition, mechanical hyperalgesia was evaluated in 3 groups of animals that were administered escalating doses of calcitonin, gabapentin or ketorolac at 48 hours intervals. At the conclusion of the experimental period the lumbar spinal cord was harvested and stained for GFAP. Compared to intact and PIN control, mechanical hyperalgesia was increased in the CF+PIN animals (p<0.01), and inhibited dose-dependently by gabapentin but not by calcitonin or ketorolac (p<0.01). Spinal GFAP sensitization was inhibited with both gabapentin and ketorolac. Interestingly, the inhibition of mechanical hyperalgesia and spinal GFAP staining by gabapentin appeared to be highly correlated. In contrast, ketorolac, which is known to delay fracture repair, inhibited spinal GFAP sensitization without alleviating mechanical hyperalgesia. In conclusion, the inhibition of persistent pain by gabapentin but not by calcitonin or ketorolac suggests that the fracture pain in this model may be neuropathic in nature. Furthermore, these findings demonstrate the potential of this model to investigate and characterize the mechanisms associated with the development of chronic bone pain following fracture.

Sample Citation:

[Authors]. [Abstract Title]. Program No. XXX.XX. 2004 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2004. Online.

Copyright © 2004-2026 Society for Neuroscience; all rights reserved. Permission to republish any abstract or part of any abstract in any form must be obtained in writing by SfN office prior to publication.

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