Difference between revisions of "Linley 2012 Proc Natl Acad Sci U S A"
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{{Publication | {{Publication | ||
|title=Linley JE, Ooi L, Pettinger L, Kirton H, Boyle JP, Peers C, Gampera N (2012) Reactive oxygen species are second messengers of neurokinin signaling in peripheral sensory neurons. Proc Natl Acad Sci U S A | |title=Linley JE, Ooi L, Pettinger L, Kirton H, Boyle JP, Peers C, Gampera N (2012) Reactive oxygen species are second messengers of neurokinin signaling in peripheral sensory neurons. Proc Natl Acad Sci U S A 109: 1578-1586 | ||
|info=[http://www. | |info=[http://www.ncbi.nlm.nih.gov/pubmed/22586118 PMID: 22586118 Open Access] | ||
|authors=Linley JE, Ooi L, Pettinger L, Kirton H, Boyle JP, Peers C, Gampera N | |authors=Linley JE, Ooi L, Pettinger L, Kirton H, Boyle JP, Peers C, Gampera N | ||
|year=2012 | |year=2012 | ||
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spontaneous pain and hyperalgesia can have distinct underlying | spontaneous pain and hyperalgesia can have distinct underlying | ||
mechanisms within a single nociceptive neuron. | mechanisms within a single nociceptive neuron. | ||
|keywords= | |keywords=Dorsal root ganglia | ||
|mipnetlab=UK Leeds Peers C, | |mipnetlab=UK Leeds Peers C, | ||
}} | }} |
Revision as of 11:33, 14 March 2013
Linley JE, Ooi L, Pettinger L, Kirton H, Boyle JP, Peers C, Gampera N (2012) Reactive oxygen species are second messengers of neurokinin signaling in peripheral sensory neurons. Proc Natl Acad Sci U S A 109: 1578-1586 |
Linley JE, Ooi L, Pettinger L, Kirton H, Boyle JP, Peers C, Gampera N (2012) Proc Natl Acad Sci U S A
Abstract: Substance P (SP) is a prominent neuromodulator, which is produced and released by peripheral damage-sensing (nociceptive) neurons; these neurons also express SP receptors. However, the mechanisms of peripheral SP signaling are poorly understood. We report a signaling pathway of SP in nociceptive neurons: Acting predominantly through NK1 receptors and Gi/o proteins, SP stimulates increased release of reactive oxygen species from the mitochondrial electron transport chain. Reactive oxygen species, functioning as second messengers, induce oxidative modification and augment M-type potassium channels, thereby suppressing excitability. This signaling cascade requires activation of phospholipase C but is largely uncoupled from the inositol 1,4,5-trisphosphate sensitive Ca2+ stores. In rats SP causes sensitization of TRPV1 and produces thermal hyperalgesia. However, the lack of coupling between SP signaling and inositol 1,4,5-trisphosphate sensitive Ca2+ stores, together with the augmenting effect on M channels, renders the SP pathway ineffective to excite nociceptors acutely and produce spontaneous pain. Our study describes a mechanism for neurokinin signaling in sensory neurons and provides evidence that spontaneous pain and hyperalgesia can have distinct underlying mechanisms within a single nociceptive neuron. β’ Keywords: Dorsal root ganglia
β’ O2k-Network Lab: UK Leeds Peers C
Labels:
Stress:RONS; Oxidative Stress"RONS; Oxidative Stress" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Rat Tissue;cell: Nervous system Preparation: Intact Cell; Cultured; Primary"Intact Cell; Cultured; Primary" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.
Coupling state: OXPHOS
HRR: Oxygraph-2k