Superficial NK1-expressing neurons control spinal excitability through activation of descending pathways
- R. Suzuki, S. Morcuende, M. Webber, S. Hunt, A. Dickenson
- BiologyNature Neuroscience
- 1 December 2002
It is concluded that NK1-positive spinal projection neurons, activated by primary afferent input, project to higher brain areas that control spinal excitability—and therefore pain sensitivity—primarily through descending pathways from the brainstem.
Diffuse noxious inhibitory controls (DNIC). I. Effects on dorsal horn convergent neurones in the rat
- D. Bars, A. Dickenson, J. Besson
- BiologyPain
- 1 June 1979
KCNQ/M Currents in Sensory Neurons: Significance for Pain Therapy
- G. Passmore, A. Selyanko, D. Brown
- BiologyJournal of Neuroscience
- 6 August 2003
It is suggested that IK(M) plays a key role in controlling the excitability of nociceptors and may represent a novel analgesic target.
The tetrodotoxin-resistant sodium channel SNS has a specialized function in pain pathways
- A. Akopian, V. Souslova, J. Wood
- BiologyNature Neuroscience
- 1 June 1999
Data show that SNS is involved in pain pathways and suggest that blockade of SNS expression or function may produce analgesia without side effects, and show that TTX-resistant sodium channel α subunit is encoded by the sns gene.
Neuropathic pain
- L. Colloca, Taylor Ludman, S. Raja
- MedicineNature Reviews Disease Primers
- 2017
Quality of life is impaired in patients with neuropathic pain owing to increased drug prescriptions and visits to health care providers, as well as the morbidity from the pain itself and the inciting disease.
Warm-coding deficits and aberrant inflammatory pain in mice lacking P2X 3 receptors
- V. Souslova, P. Cesare, J. Wood
- BiologyNature
- 26 October 2000
It is demonstrated that ablation of the P2X3 gene results in the loss of rapidly desensitizing ATP-gated cation currents in dorsal root ganglion neurons, and that the responses of nodose ganglions neurons to ATP show altered kinetics and pharmacology resulting from the lost expression of P2 X2/3 heteromultimers.
The Cell and Molecular Basis of Mechanical, Cold, and Inflammatory Pain
- B. Abrahamsen, J. Zhao, J. Wood
- BiologyScience
- 1 August 2008
These data demonstrate that Nav1.8-expressing neurons are essential for mechanical, cold, and inflammatory pain but not for neuropathic pain or heat sensing, and kill all mouse postmitotic sensory neurons expressing the sodium channel Nav 1.8.
Nociceptor-specific gene deletion reveals a major role for Nav1.7 (PN1) in acute and inflammatory pain.
- M. Nassar, L. Stirling, J. Wood
- BiologyProceedings of the National Academy of Sciences…
- 24 August 2004
All inflammatory pain responses evoked by a range of stimuli, such as formalin, carrageenan, complete Freund's adjuvant, or nerve growth factor, were reduced or abolished and should prove useful in understanding the role of other broadly expressed genes in pain pathways.
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