Difference between revisions of "Linley 2012 Proc Natl Acad Sci U S A"
Bader Helga (talk | contribs) Β |
|||
(9 intermediate revisions by 2 users not shown) | |||
Line 1: | Line 1: | ||
{{Publication | {{Publication | ||
|title=Linley JE, Ooi L, Pettinger L, Kirton H, Boyle JP, | |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 109:1578-86 | ||
|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, | |authors=Linley JE, Ooi L, Pettinger L, Kirton H, Boyle JP, Peers C, Gampera N | ||
|year=2012 | |year=2012 | ||
|journal=Proc Natl Acad Sci U S A | |journal=Proc Natl Acad Sci U S A | ||
Line 17: | Line 17: | ||
excitability. This signaling cascade requires activation of phospholipase | excitability. This signaling cascade requires activation of phospholipase | ||
C but is largely uncoupled from the inositol 1,4,5-trisphosphate | C but is largely uncoupled from the inositol 1,4,5-trisphosphate | ||
sensitive | sensitive Ca<sup>2+</sup> stores. In rats SP causes sensitization of TRPV1 | ||
and produces thermal hyperalgesia. However, the lack of coupling | and produces thermal hyperalgesia. However, the lack of coupling | ||
between SP signaling and inositol 1,4,5-trisphosphate sensitive | between SP signaling and inositol 1,4,5-trisphosphate sensitive Ca<sup>2+</sup> | ||
stores, together with the augmenting effect | stores, together with the augmenting effect on M channels, renders | ||
the SP pathway ineffective to excite nociceptors acutely and produce | the SP pathway ineffective to excite nociceptors acutely and produce | ||
spontaneous pain. Our study describes a mechanism for neurokinin | spontaneous pain. Our study describes a mechanism for neurokinin | ||
Line 26: | Line 26: | ||
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, | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|organism=Rat | |||
|tissues=Nervous system | |||
|preparations=Intact cells | |||
|injuries=Oxidative stress;RONS | |||
|couplingstates=OXPHOS | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} |
Latest revision as of 16:38, 23 February 2015
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 109:1578-86 |
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:Oxidative stress;RONS Organism: Rat Tissue;cell: Nervous system Preparation: Intact cells
Coupling state: OXPHOS
HRR: Oxygraph-2k