title: Tumor Necrosis Factor-α Suppresses Activation of Sustained Potassium Currents in Rat Small Diameter Sensory Neurons.
abstract: Tumor necrosis factor-α (TNF-α), a pro-inflammatory cytokine, produces pain and hyperalgesia by activating and/or sensitizing nociceptive sensory neurons. In the present study, using whole-cell patch clamp techniques, the regulation of potassium currents by TNF-α was examined in acutely dissociated small dorsal root ganglion neurons. We found that acute application of TNF-α inhibited, in a dose-dependent manner, the non-inactivating sustained potassium current without changing the rapidly inactivating transient current or the kinetics of steady-state inactivation. The effects of TNF-α on potassium currents were similar to that of prostaglandin E2 as reported previously and also demonstrated in the current study. Furthermore, indomethacin, a potent inhibitor for both cyclo-oxygenase (COX) -1 and COX-2, completely blocked the effect of TNF-α on potassium currents. These results suggest that TNF-α may sensitize or activate sensory neurons by suppressing the sustained potassium current in nociceptive DRG neurons, possibly via stimulating the synthesis/release of endogenous prostaglandins.
authors.affiliation: Department of Anesthesiology, University of Arkansas for Medical Sciences, Little Rock, AR.
authors.forename: Bao-Gang
authors.initials: BG
authors.lastname: Liu
authors.forename: Maxim
authors.initials: M
authors.lastname: Dobretsov
authors.forename: Joseph R
authors.initials: JR
authors.lastname: Stimers
authors.forename: Jun-Ming
authors.initials: JM
authors.lastname: Zhang