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Fig. 2 | Cell Communication and Signaling

Fig. 2

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. 2

CCK-8 decreased IA via activation of CCK-BR. a, western blot analysis demonstrated the expression of CCK-AR and CCK-BR protein in mouse DRGs. GAPDH is shown as loading control. Representative western blots are shown from at least three independent experiments. b, co-localization of CCK-BR (Red) with three markers (Green) (CGRP, IB4, and NF-200) in naïve mouse DRGs. Arrows show the co-localization. Scale bars: 30 μm. c, d, time course of changes in IA amplitude mediated by 100 nM CCK-8 in the presence of either devazepide (1 μM, n = 10, c) or LY225910 (1 μM, n = 8, d). Insets show the exemplary current traces. The Arabic numerals indicate the relative points utilized for exemplary current traces. e, bar graph showing that treatment of DRG neurons with LY225910, instead of devazepide, abrogated the CCK-8-induced IA response. f, bar graph showing that application of BC264 (0.1 μM, n = 7) or CCK-4 (300 nM, n = 7), but not GW5823 (5 μM, n = 9), significantly decrease IA in small DRG neurons. *p < 0.05 and **p < 0.01 vs. control

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