Voltage-gated potassium channels are regulators of membrane potentials, action potential shape, firing adaptation, and neuronal excitability in excitable tissues including in the primary sensory neurons of dorsal root ganglion (DRG). In this study, using the whole-cell patch-clamp technique, the effect of estradiol (E2) on voltage-gated total outward potassium currents, the component currents transient “A-type” current (I A) currents, and “delayed rectifier type” (I KDR) currents in isolated mouse DRG neurons was examined. We found that the extracellularly applied 17β-E2 inhibited voltage-gated total outward potassium currents; the effects were rapid, reversible, and concentration-dependent. Moreover, the membrane impermeable E2-BSA was as efficacious as 17β-E2, whereas 17α-E2 had no effect. 17β-E2-stimulated decrease in the potassium current was unaffected by treatment with ICI 182780 (classic estrogen receptor antagonist), actinomycin D (RNA synthesis inhibitor), or cycloheximide (protein synthesis inhibitor). We also found that I A and I KDR were decreased after 17β-E2 application. 17β-E2 significantly shifted the activation curve for I A and I KDR channels in the hyperpolarizing direction. In conclusion, our results demonstrate that E2 inhibited voltage-gated K+ channels in mouse DRG neurons through a membrane ER-activated non-genomic pathway.
The Journal of Membrane Biology – Springer Journals
Published: May 17, 2014
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