作者: Charles L. Rodriguez-Feo , Kevin W. Sexton , Richard B. Boyer , Alonda C. Pollins , Nancy L. Cardwell
DOI: 10.1016/J.JSS.2013.04.082
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摘要: Abstract Background Activation of the P2X7 receptor on peripheral neurons causes formation pannexin pores, which allows influx calcium across cell membrane. Polyethylene glycol (PEG) and methylene blue have previously been shown to delay Wallerian degeneration if applied during microsuture repair severed nerve. Our hypothesis is that by modulating via pathway, we could improve PEG-based axonal repair. The can be stimulated or inhibited using bz adenosine triphosphate (bzATP) brilliant (FCF), respectively. Methods A single incision rat sciatic nerve injury model was used. defect repaired a described PEG fusion protocol. Experimental animals were treated with 100 μL 100 μM FCF solution ( n = 8) 30 μM bzATP 6). Control received no FCF, bzATP, PEG. Compound action potentials recorded prior transection (baseline), immediately after repair, 21 d postoperatively. Animals underwent behavioral testing 3, 7, 14, After sacrifice, nerves fixed, sectioned, immunostained allow for counting total axons. Results Rats showed an improvement compared control at all time points P = 0.047, 0.044, 0.014, 0.0059, respectively). statistical difference was also between d 7 > 0.05). Conclusions Blocking improves functional outcomes PEG-mediated fusion.