Figure 7.

tDrysdalin inhibition of nAChRs subtypes. A, Bar graph of tDrysdalin (100 nmol/L) inhibition of ACh‐evoked peak current amplitude mediated by rα1β1δε, hα7, hα9α10, hα3β2, hα3β4, hα4β2, and hα4β4 nAChRs. Whole‐cell currents at hα3β2 and hα4β2 were activated by 6 µmol/L ACh, hα3β4, hα4β4, hα7, and rα1β1δεnAChRs were activated by 300, 3, 200, and 1 µmol/L ACh, respectively (mean ± SEM, n = 3‐6) (unpaired Student t test; *P < 0.0001 vs relative current amplitude of 1). B, Representative ACh (1 μmol/L)‐evoked currents recorded from Xenopus oocytes expressing rodent muscle α1β1δε nAChRs in the absence (control) and presence of 1‐300 nmol/L tDrysdalin (top row), and following washout between applications of tDrysdalin (bottom row). C, Concentration‐response curve of the relative ACh‐evoked current amplitude mediated by rα1β1δε nAChRs in the presence of tDrysdalin gave an IC₅₀ of 97.4 ± 14 nmol/L (n = 3) and 1.3 as Hill coefficient (n^H). D, Representative ACh (200 μmol/L)‐evoked currents recorded from oocytes expressing human(h)α7 nAChR in the absence (control) and presence of 1‐300 nmol/L tDrysdalin (top row), and following washout between applications of tDrysdalin (bottom row). E, Concentration‐response curve of the relative ACh‐evoked current amplitude mediated by hα7 nAChRs in the presence of tDrysdalin gave an IC₅₀ of 19.5 ± 2.1 nmol/L (n = 3) and n^H of 1.3