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M-type K+ channel as plasma membrane nitric oxide and reactive oxygen species sensor

Journal Article


Abstract


  • M-type K+ channels control excitability of many neuron types. M channel activity is potently enhanced by oxidative modification of triple cysteine pocket within the cytosolic linker between transmembrane domains 2 and 3. Thus, in sensory neurons from dorsal root (DRG) and trigeminal (TG) ganglia M channel activity is increased by the mitochondrial release of reactive oxygen species (ROS) induced by neuromodulator substance P. Here we identified a new signalling role for nitric oxide (NO) in TG sensory neurons.

Authors


  •   Ooi, Lezanne
  •   Pettinger, Louisa (external author)
  •   Gamper, Nikita (external author)

Publication Date


  • 2013

Citation


  • Ooi, L., Pettinger, L. & Gamper, N. (2013). M-type K+ channel as plasma membrane nitric oxide and reactive oxygen species sensor. Biophysical Journal, 104 (2, Suppl. 1), 268a-269a.

Start Page


  • 268a

End Page


  • 269a

Volume


  • 104

Issue


  • 2, Suppl. 1

Place Of Publication


  • United States

Abstract


  • M-type K+ channels control excitability of many neuron types. M channel activity is potently enhanced by oxidative modification of triple cysteine pocket within the cytosolic linker between transmembrane domains 2 and 3. Thus, in sensory neurons from dorsal root (DRG) and trigeminal (TG) ganglia M channel activity is increased by the mitochondrial release of reactive oxygen species (ROS) induced by neuromodulator substance P. Here we identified a new signalling role for nitric oxide (NO) in TG sensory neurons.

Authors


  •   Ooi, Lezanne
  •   Pettinger, Louisa (external author)
  •   Gamper, Nikita (external author)

Publication Date


  • 2013

Citation


  • Ooi, L., Pettinger, L. & Gamper, N. (2013). M-type K+ channel as plasma membrane nitric oxide and reactive oxygen species sensor. Biophysical Journal, 104 (2, Suppl. 1), 268a-269a.

Start Page


  • 268a

End Page


  • 269a

Volume


  • 104

Issue


  • 2, Suppl. 1

Place Of Publication


  • United States