Role of actin filaments in allodynia induced by chronic compression of the dorsal root ganglion.

Abstract

The role of actin filaments in allodynia induced by chronic compression of the dorsal root ganglion (DRG) (CCD) and the effects of microfilaments dynamics on transient receptor potential vanilloid 4 (TRPV4) were investigated in this study. Anti-microfilaments agents resulted in dose-dependent and partial reduction in CCD-induced allodynia, which could be prevented by the prior stabilizer administration. In association with the reduction of allodynia by microfilaments' disruption, TRPV4-mediated currents were inhibited by disruptors. In addition, plasma membrane-associated TRPV4 was also depressed by disruptors. The time courses for the changes of TRPV4 activity and distribution in vitro were similar to the time courses for the attenuation of allodynia in vivo. Phalloidin, the stabilizer of microfilaments, did not affect the allodynia in CCD rats. However, phalloidin resulted in reduction and delay of TRPV4 current, which was not consistent with the effect of phalloidin on CCD-induced allodynia. In accordance with the inhibition of TRPV4 activity, the reversal potentials shifted toward more positive voltages and the plasma membrane-associated TRPV4 was depressed by phalloidin. In conclusion, intact actin filaments were necessary for CCD-induced allodynia, and disruptors of microfilaments attenuated CCD-induced allodynia. However, stabilizer of actin filaments did not affect allodynia in CCD rats. Further, TRPV4 contributed to the disruptors-induced attenuation of allodynia in CCD rats.

• Authors: Hui Wei, Li-Ping Ning, Yang Zhang, Shou-Wei Yue
• Journal: Neuroscience letters (Neurosci Lett) Vol. 600 Pg. 38-44 (Jul 23 2015) ISSN: 1872-7972 [Electronic] Ireland
• PMID: 25962822 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

Chemical References

• TRPV Cation Channels
• Trpv4 protein, rat

Topics

• Actin Cytoskeleton (physiology)
• Animals
• Cell Survival
• Cells, Cultured
• Chronic Disease
• Ganglia, Spinal (injuries, metabolism, pathology)
• Hyperalgesia (etiology, metabolism, pathology)
• Male
• Neurons, Afferent (metabolism, pathology)
• Rats, Wistar
• TRPV Cation Channels (metabolism)