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Bockhart, Vanessa; Constantin, Cristina Elena; Häussler, Annett; Wijnvoord, Nina; Kanngiesser, Maike; Myrczek, Thekla; Pickert, Geethanjali; Popp, Laura; Sobotzik, Jürgen-Markus; Pasparakis, Manolis; Kuner, Rohini; Geisslinger, Gerd; Schultz, Christian; Kress, Michaela; Tegeder, Irmgard

Inhibitor κB Kinase β Deficiency in Primary Nociceptive Neurons Increases TRP Channel Sensitivity

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  • Media type: E-Article
  • Title: Inhibitor κB Kinase β Deficiency in Primary Nociceptive Neurons Increases TRP Channel Sensitivity
  • Contributor: Bockhart, Vanessa; Constantin, Cristina Elena; Häussler, Annett; Wijnvoord, Nina; Kanngiesser, Maike; Myrczek, Thekla; Pickert, Geethanjali; Popp, Laura; Sobotzik, Jürgen-Markus; Pasparakis, Manolis; Kuner, Rohini; Geisslinger, Gerd; Schultz, Christian; Kress, Michaela; Tegeder, Irmgard
  • imprint: Society for Neuroscience, 2009
  • Published in: The Journal of Neuroscience
  • Language: English
  • DOI: 10.1523/jneurosci.1496-09.2009
  • ISSN: 0270-6474; 1529-2401
  • Keywords: General Neuroscience
  • Origination:
  • Footnote:
  • Description: <jats:p>Inhibitor κB kinase (IKK) regulates the activity of the transcription factor nuclear factor-κ B that normally protects neurons against excitotoxicity. Constitutively active IKK is enriched at axon initial segments and nodes of Ranvier (NR). We used mice with a Cre–loxP-mediated specific deletion of IKKβ in sensory neurons of the dorsal root ganglion (<jats:italic>SNS–IKK</jats:italic>β<jats:sup>−/−</jats:sup>) to evaluate whether IKK plays a role in sensory neuron excitability and nociception. We observed increased sensitivity to mechanical, cold, noxious heat and chemical stimulation in<jats:italic>SNS–IKK</jats:italic>β<jats:sup>−/−</jats:sup>mice, with normal proprioceptive and motor functions as revealed by gait analysis. This was associated with increased calcium influx and increased inward currents in small- and medium-sized primary sensory neurons of<jats:italic>SNS–IKK</jats:italic>β<jats:sup>−/−</jats:sup>mice during stimulation with capsaicin or Formalin, specific activators of transient receptor potentials TRPV1 and TRPA1 calcium channels, respectively.<jats:italic>In vitro</jats:italic>stimulation of saphenous nerve preparations of<jats:italic>SNS–IKK</jats:italic>β<jats:sup>−/−</jats:sup>mice showed increased neuronal excitability of A- and C-fibers but unchanged A- and C-fiber conduction velocities, normal voltage-gated sodium channel currents, and normal accumulation of ankyrin G and the sodium channels Nav1.6 at NR. The results suggest that IKKβ functions as a negative modulator of sensory neuron excitability, mediated at least in part by modulation of TRP channel sensitivity.</jats:p>
  • Access State: Open Access