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Fig. 4 | Cell Communication and Signaling

Fig. 4

From: Cholecystokinin type B receptor-mediated inhibition of A-type K+ channels enhances sensory neuronal excitability through the phosphatidylinositol 3-kinase and c-Src-dependent JNK pathway

Fig. 4

The CCK-BR-mediated IA decrease requires PI3K, but not Akt. a, time course of changes in IA amplitude (left) and summary data (right) showing the effects of 100 nM CCK-8 on IA in the presence of GF109203X (1 μM for 30 min, n = 9). Insets show the representative current traces. The numbers on the plot indicate which points were used for sample traces. b, representative traces (left) and bar graph (right) indicating the effect of 5 μM PMA on IA in the absence (n = 5) or presence (n = 9) of 1 μM GF109203X. c, pretreating cells with 20 μM LY294002 prevented the CCK-8-induced increase in PI3K activity. The experiments were conducted in triplicate and yielded with similar results. d, e, time course showing the effect of CCK-8 (100 nM) on IA in the presence of LY294002 (20 μM for 30 min, d) or wortmannin (1 μM for 30 min, e). Insets show exemplary current traces. The Arabic numerals indicate the relative points utilized for exemplary current traces. f, bar graph showing the effects of CCK-8 on IA in the presence of LY294002 (n = 8) or wortmannin (n = 10) indicated in panels d and e respectively. g, CCK-8 induced a significant increase in the phosphorylated Akt (p-Akt) in DRG cells. This effect was abrogated by pretreating cells with LY294002 (20 μM for 30 min) or the Akt inhibitor III (10 μM for 30 min). h, left: representative traces and time course indicating the inhibitory effects of 100 nM CCK-8 on IA in the presence of Akt inhibitor III (10 μM). Insets show exemplary current traces. The Arabic numerals indicate the relative points utilized for exemplary current traces. Right: bar graph showing that treatment of DRG neurons with Akt inhibitor III (n = 9) had no effect on the CCK-8–induced IA response. **p < 0.01 and ***p < 0.001 vs. control

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