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. Author manuscript; available in PMC: 2021 Sep 1.
Published in final edited form as: Pain. 2020 Sep 1;161(9):2179–2190. doi: 10.1097/j.pain.0000000000001905

Figure 7.

Figure 7.

Effects of the adenosine A3R agonists Cl-IB-MECA and MRS5950 on voltage-gated Ca2+ currents in isolated DRG neurons. (A) Time course (left panel) and representative Ca2+ current traces (right panel) measured in a representative DRG neuron isolated from a DNBS-treated rat (DNBS) before and after the application of the A3R agonist Cl-IB-MECA (30 nM) or the Ca2+ channel blocker Cd2+ (100 μM). (B) Averaged time courses of peak Ca2+ currents during Cl-IB-MECA (30 nM) superfusion in vehicle-treated or DNBS-treated animals in the absence or presence of the A3AR antagonist, MRS1523 (1523: 100 nM). Pooled data (mean ± SEM) of % Ca2+ current inhibition induced by Cl-IB-MECA (C) or MRS5980 (D) applied alone or in combination with MRS1523 or PD173232 (PD; 1 μM) in vehicle-treated (white columns) or DNBS-treated (red columns) animals. In all panels: *P <0.05 vs respective control, paired Student t test. (E) Averaged time course of peak Ca2+ currents before or after MRS5980 (30 nM) superfusion DNBS rats in the presence of the A3AR antagonist MRS1523 or the Ca2+ channel blocker PD173232 (1 μM). DRG, dorsal root ganglia.