Skip to main content
Figure 4 | Molecular Pain

Figure 4

From: Transforming growth factor beta induces sensory neuronal hyperexcitability, and contributes to pancreatic pain and hyperalgesia in rats with chronic pancreatitis

Figure 4

a. Representative K+ currents in DRG neurons treated with TGFβ1. Step depolarizations from −60 to +30 mV in 5-mV increments (duration = 400 ms, holding potential = −100 mV) were used to activate all Kv channels (Itotal) in cultured DRG neurons with or without exposure to TGFβ for 48 hours (left column, top two rows). Manipulating the holding potential to –50 mV with the same depolarization steps activated most of the sustained Kv channels but not IA channels (middle column, top two rows). Subtraction of IK from Itotal yields IA (right column, top two rows). The peak I-V curves for IA are shown in the bottom row. b. Quantification of IK (top) and IA (middle) currents in TGFβ1-treated and control neurons. TGFβ1 treatment resulted in a significant reduction in IA density at +30 mV (28.58 ± 3.958, n = 25 versus 68.67 ± 11.95 n = 17) but not in IK density. The bottom panels shows the normalized conductance (G/V relationship) for IA currents in control (n = 7) and TGFβ1 treated neurons (n = 10). c. Changes in KCNA4 expression in response to TGFβ1. Top: mRNA expression in DRG cultures treated with TGFβ1, expressed relative to GAPDH mRNA expression. Middle: Representative immunohistochemistry images from control and TGFβ1 treated cultures. Bottom: Bar graph showing relative intensity of cell fluorescence (averaged per high power field) showing significant decrease after 48 hours of exposure to TGFβ1 as compared with controls (854.3 ± 84.61, n = 11 fields versus 11348.3 ± 25.47, n = 8 fields). ** P < 0.01; ***P < 0.001.

Back to article page