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Impaired nociception and pain sensation in mice lacking the capsaicin receptor.
Sensory neurons from mice lacking VR1 are severely deficient in their responses to each of these noxious stimuli and are impaired in the detection of painful heat, and showed little thermal hypersensitivity in the setting of inflammation.
Methylglyoxal modification of Nav1.8 facilitates nociceptive neuron firing and causes hyperalgesia in diabetic neuropathy
It is found that concentrations of plasma methylglyoxal above 600 nM discriminate between diabetes-affected individuals with pain and those without pain, which provides a new basis for the design of therapeutic interventions for painful diabetic neuropathy.
Sensory neuron sodium channel Nav1.8 is essential for pain at low temperatures
This work shows that cooling excitable membranes progressively enhances the voltage-dependent slow inactivation of tetrodotoxin-sensitive VGSCs, and presents strong evidence for a specialized role of Nav1.8 in nociceptors as the critical molecule for the perception of cold pain and pain in the cold.
The vanilloid receptor TRPV1 is activated and sensitized by local anesthetics in rodent sensory neurons.
Lidocaine activation is sufficient to release CGRP, a key component of neurogenic inflammation, and warrants investigation into the role of TRPV1 and TRPA1 in LA-induced neurotoxicity.
H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO–TRPA1–CGRP signalling pathway
It is proposed that this neuroendocrine HNO–TRPA1–CGRP signalling pathway constitutes an essential element for the control of vascular tone throughout the cardiovascular system.
Methylglyoxal Activates Nociceptors through Transient Receptor Potential Channel A1 (TRPA1)
- M. Eberhardt, M. Filipovic, S. Sauer
- Biology, MedicineThe Journal of Biological Chemistry
- 27 June 2012
Methylglyoxal is proposed to be a candidate metabolite that causes neuropathic pain in metabolic disorders and thus is a promising target for medicinal chemistry.
The role of the capsaicin receptor TRPV1 and acid-sensing ion channels (ASICS) in proton sensitivity of subpopulations of primary nociceptive neurons in rats and mice
TRPA1 and substance P mediate colitis in mice.
Activation and sensitization of TRPA1 and release of substance P induce and maintain colitis in mice and neuroimmune interactions control intestinal inflammation.
Sodium channelopathies and pain
- A. Lampert, A. O’Reilly, P. Reeh, A. Leffler
- BiologyPflügers Archiv - European Journal of Physiology
- 26 January 2010
This review aims to cover recent progress on the understanding of how biophysical properties of mutant Nav1.7 translate into an aberrant electrogenesis of nociceptors and recapitulate the role ofNav1.8 for peripheral pain processing and of additional sodium channelopathies which have been linked to disorders with pain as a significant component.
Human TRPA1 is a heat sensor displaying intrinsic U-shaped thermosensitivity
It is shown that redox modification and ligands affect human TRPA1 (hTRPA1) cold and heat sensing properties in lipid bilayer and whole-cell patch-clamp recordings as well as heat-evoked TRPA 1-dependent calcitonin gene-related peptide (CGRP) release from mouse trachea.