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Fig. 6 | Cell Communication and Signaling

Fig. 6

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. 6

CCK-8 induces neuronal hyperexcitability. a-c exemplary current traces (left) and bar graph (right) indicating the effect of 100 nM CCK-8 on Nav currents (INa, n = 11, A), high-voltage-activated Cav currents (IBa of HVGCC, n = 8, b), or low-voltage-activated Cav currents (IBa of LVGCC, n = 9, c), respectively. Either Nav currents or IBa of HVGCC were elicited by a test pulse to 0 mV from a holding potential of − 60 mV. A stepped voltage protocol from − 110 to − 40 mV with a holding potential of − 110 mV was applied to elicit IBa of LVGCC. d, e exemplary traces (d) and summary of results (e, n = 17) indicating the effect of CCK-8 (100 nM) on action potential firing rate. Representative traces were recorded when small-sized DRG neurons were subjected to 130 pA current injections. f, g CCK-8 at 100 nM significantly shortened first spike latency (f) and decreased the AP threshold (g) in small-sized DRG neurons (n = 17). h, i representative traces (h) and summary of results (i) showing that pretreatment of cells with LY225910 (1 μM, n = 12) abolished the 100 nM CCK-8-induced the increase in firing rate. Representative traces were recorded when small-sized DRG neurons were subjected to 130 pA current injections. j, k exemplary current traces (j) and summary of results (k) indicating that application of 4-AP at 5 mM abrogated the 100 nM CCK-8-induced neuronal hyperexcitability (n = 12). Representative traces were recorded when small-sized DRG neurons were subjected to 80 pA current injections. *p < 0.05 and **p < 0.01 vs. control

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