| 0703 Sodium Channel Expression in an Animal Model for Trigeminal Neuralgia | ||
|
F.W. STARK1, G.M. PERRY1, L.R. JOHNSON2, S.R. LEVINSON2, and M.A. HENRY1, 1University of Texas Health Science Center at San Antonio, USA, 2University of Colorado Health Sciences Center, Aurora, USA Trigeminal neuralgia (TN) is one of the most painful conditions known to humans whose mechanisms are not fully understood. One proposed mechanism involves a demyelinating lesion of the trigeminal central root secondary to vascular compression and reorganization of ion channels in demyelinated nerves resulting in increased excitability. Clinical experience suggests this reorganization involves sodium channels (NaChs) since NaCh-blocking medications show efficacy in treatment of TN pain. Objective: Evaluate placement of a chromic suture lesion in the central root on NaCh expression as a possible animal model of TN. Methods: Chromic sutures were placed into the central root of five rats. Two-three weeks later experimental and two control subjects were tested for head withdrawal in response to mechanical/brush stimulus and then sacrificed. Trigeminal ganglion (TG) sections were double-labeled with NaCh and caspr (paranodal protein used to identify nodes) antibodies using indirect immunofluorescence and confocal microscopy. Multiple Z-series were obtained and evaluated with NIH ImageJ software to determine NaCh accumulation average size and their associations at caspr-identified nodal sites. Results: Experimental subjects showed head withdrawal to facial brush stimulus when applied to the side with the suture. Relative to controls, chromic suture lesion resulted in decreased occurrence of typical nodes (90.9% vs. 56.2%), increased occurrence of altered caspr-NaCh relationships that result from demyelination (heminodes- 2.8 vs. 17.7%; naked NaCh accumulations- 5.4 vs. 23.6%), and a significant augmentation of NaChs in all nodal forms. Conclusion: The placement of chromic suture into the central root results in behavior demonstrating sensitivity to mechanical stimulation, and a demyelinating lesion and reorganization of NaChs at these sites, thus reproducing key findings of TN seen in humans. These findings suggest this animal model may be useful to further explore basic mechanisms associated with the pathogenesis of TN. This work was supported by NIDCR, Grants #DE14318/COSTAR Program and #DE13942/M.Henry.
| ||
| Seq #96 - TMD and orofacial pain mechanisms 2:00 PM-3:15 PM, Thursday, March 22, 2007 Ernest N. Morial Convention Center Exhibit Hall I2-J | ||
|
Back to the Neuroscience / TMJ Program
| ||