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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 doi/10.1073/pnas.1201544109.
|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.pnas.org/content/early/2012/05/11/1201544109.full.pdf+html doi/10.1073/pnas.1201544109]
|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=dorsal root ganglia
|keywords=Dorsal root ganglia
|mipnetlab=UK Leeds Peers C,
|mipnetlab=UK Leeds Peers C,
}}
}}

Revision as of 10:33, 14 March 2013

Publications in the MiPMap
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

Β» PMID: 22586118 Open Access

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