Fig. 7: Effect of knockdown of TRP-2, and GON-2 + CED-11 TRP channels on the DEC activated inward currents with control acetylcholine (ACh), and emodepside (emd) current-responses.
From: Diethylcarbamazine activates TRP channels including TRP-2 in filaria, Brugia malayi
a Control worms: inward currents induced in the presence of 5 mM 4AP by 30 µM DEC (−653 ± 81 pA, n = 8 muscles) and acetylcholine induced (−1716 ± 36 pA, n = 8). In absence of 4AP, emodepside produced outward current (846 ± 69 pA, n = 8 muscles). b TRP-2 dsRNA knockdown worms: currents induced in the presence of 5 mM 4AP, 30 µM DEC (−14.5 ± 1.5 pA, n = 8) and ACh induced (−1590 ± 185 pA, n = 8) inward currents. In absence of 4AP, emodepside produced outward current (756 ± 47 pA, n = 8). Note the striking inhibition following TRP-2 knockdown. c GON-2+CED-11 dsRNA knockdown worms: currents induced in the presence of 5 mM 4AP, 30 µM DEC (−300 ± 24 pA, n = 8) and ACh induced (−1570 ± 217 pA, n = 8) inward currents. In the absence of 4AP, emodepside produced outward currents (732 ± 34.6 pA, n = 8). d Box-whisker plot demonstrating the effect of different dsRNA treatments on DEC, ACh, and emodepside induced currents. The inward DEC currents were significantly inhibited by the TRP-2 knockdown and the CED-11+GON-2 knockdown. The biggest effect was observed for the TRP-2 knockdown (one-way ANOVA with Bonferroni post-hoc test; p < 0.0001, 95% confidence interval for control vs. gon-2 + ced-11 was −571.6 to −134.2 and for control vs. trp-2 was −857.2 to −419.9; n = 5 from five worms).
