Figure 1.

Insulin and IGF-I potentiate TRPV1 currents in Xenopus Oocytes. a, A representative dual-electrode whole-oocyte experiment showing potentiation of capsaicin induced TRPV1 currents following 15 min incubation of insulin (see Methods). b, Time course for capsaicin induced current (■: 500 nM capsaicin, 30 sec application) before and after insulin exposure at 5 (P < .05), 10 (P < .01), and 15 min (P < .01) incubation times (n = 7). c, Dose response curve of capsaicin before (squares) and after 5 μM insulin (circles) application, the currents were normalized to 1 μM capsaicin before insulin application (n = 2 to 4, before and after insulin). Both the sensitivity (EC50 shifted from 0.9 to 0.6 μM) and maximal response increased (1.8 to 2.4). d, Representative I-V relationships (1 s, 1 mV step ramp from -80 to +80 mV) before and after insulin treatment that demonstrates the outward rectification typical of TRPV1 channels. e, Potentiation of heat-induced currents by insulin. f, Potentiation of pH induced currents by insulin. g, Potentiation of pH induced currents by IGF-I. h, Tyrphostin A47, an IR / IGFR antagonist, blocked insulin potentiation. i, Summary graph showing fold increase in TRPV1 currents following 10 min incubation with control, insulin (cap: n = 5, P < .01; pH: n = 4, P < .01), IGF-I (n = 3, P < .01), and insulin + tyrophostin A47 (n = 3, P < .01). Results are expressed as increase in current amplitude relative to initial capsaicin or pH response.

Van Buren et al. Molecular Pain 2005 1:17   doi:10.1186/1744-8069-1-17
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