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

• Disruption of actin filaments results in reduction in CCD-induced allodynia.
• Disruption of actin filaments results in inhibition of TRPV4-mediated currents.
• Disruption of actin filaments inhibits the plasma membrane-associated TRPV4.
• Intact actin filaments are necessary for CCD-induced allodynia.
• TRPV4 contributes to the relief of allodynia induced by disruptors’ treatment.

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.