Skip to main content
. 2015 Sep;146(3):205–219. doi: 10.1085/jgp.201511383

Figure 1.

Figure 1.

Constitutive and ghrelin-dependent GHSR1a activity inhibit CaV2 currents. (A) Representative ICa traces from HEK 293T cells transfected with CaV2.1 or CaV2.2, CaVα2δ1, CaVβ3, and 0.6 µg GHSR1a, GHSR1a-A204E, or empty pcDNA3.1+ (control), and averaged ICa at different amounts of GHSR1a plasmid transfected. (B) Representative microphotographs (left) and average fluorescent signal intensity (right) for the F-ghrelin binding in cells transfected with increasing amounts of GHSR1a plasmid. (C) Representative ICa traces from cells cotransfected with CaV2.1 and CaV2.2, CaVα2δ1, CaVβ3, and 0.6 µg GHSR1a or GHSR1a-A204E with or without 1 µM SPA preincubation (left), and the averaged ICa for each condition (right). (D) Time courses and representative traces of ghrelin effect on ICa from cells expressing CaV2.1 or CaV2.2, CaVα2δ1, CaVβ3, and GHSR1a-A204E (left), and the averaged percentage of CaV2.1 and CaV2.2 current inhibition at different amounts of GHSR1a plasmid transfected. ANOVA with Dunnett’s (C) and Tukey’s post-test (D). *, P < 0.05. Error bars represent mean ± SE.