Figure 2.
Figure 2. Stably expressed human Cav2.1 (α1A-2) or human Cav2.3c (α1E-c) channel inhibition by baclofen (bac) and α-conotoxin Vc1.1 in the absence and presence of transiently expressed human GABABR. (A and C) Bar graphs showing average IBa inhibition through Cav2.1 (A) or Cav2.3c (C) channels by 50 µM baclofen, 200 nM Vc1.1, or 200 nM c-Vc1.1. Numbers in parentheses indicate the number of experiments. (E) Average IBa inhibited by 50 µM baclofen applied before or after 200 nM c-Vc1.1; “before c-Vc1.1” data are replotted from C. (B, D, and F) Concentration-dependent inhibition of IBa through Cav2.1 and Cav2.3c channels by baclofen (B and D) and Cav2.3c channels by c-Vc1.1 (F). See IC50 values in Table 2.

Stably expressed human Cav2.1 (α1A-2) or human Cav2.3c (α1E-c) channel inhibition by baclofen (bac) and α-conotoxin Vc1.1 in the absence and presence of transiently expressed human GABABR. (A and C) Bar graphs showing average IBa inhibition through Cav2.1 (A) or Cav2.3c (C) channels by 50 µM baclofen, 200 nM Vc1.1, or 200 nM c-Vc1.1. Numbers in parentheses indicate the number of experiments. (E) Average IBa inhibited by 50 µM baclofen applied before or after 200 nM c-Vc1.1; “before c-Vc1.1” data are replotted from C. (B, D, and F) Concentration-dependent inhibition of IBa through Cav2.1 and Cav2.3c channels by baclofen (B and D) and Cav2.3c channels by c-Vc1.1 (F). See IC50 values in Table 2.

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