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.
Cellular and Molecular Mechanisms of Pain
The Cloned Capsaicin Receptor Integrates Multiple Pain-Producing Stimuli
TRPA1 Mediates the Inflammatory Actions of Environmental Irritants and Proalgesic Agents
Bradykinin and nerve growth factor release the capsaicin receptor from PtdIns(4,5)P2-mediated inhibition
It is shown that bradykinin- or NGF-mediated potentiation of thermal sensitivity in vivo requires expression of VR1, a heat-activated ion channel on sensory neurons, and biochemical studies suggest that VR1 associates with this complex.
Molecular mechanisms of nociception
Efforts to determine how primary sensory neurons detect pain-producing stimuli of a thermal, mechanical or chemical nature have revealed new signalling mechanisms and brought us closer to understanding the molecular events that facilitate transitions from acute to persistent pain.
Endogenous pain control systems: brainstem spinal pathways and endorphin circuitry.
The menthol receptor TRPM8 is the principal detector of environmental cold
It is shown that cultured sensory neurons and intact sensory nerve fibres from TRPM8-deficient mice exhibit profoundly diminished responses to cold, validating the hypothesis that TRP channels are the principal sensors of thermal stimuli in the peripheral nervous system.
Distinct subsets of unmyelinated primary sensory fibers mediate behavioral responses to noxious thermal and mechanical stimuli
- D. J. Cavanaugh, Hyosang Lee, David J. Anderson
- Biology, PsychologyProceedings of the National Academy of Sciences
- 2 June 2009
Evidence is provided that the brain can distinguish different noxious stimulus modalities from the earliest stages of sensory processing, and that combined elimination of both populations yielded an additive phenotype with no additional behavioral deficits, ruling out a redundant contribution of these populations to heat and mechanical pain sensitivity.
Injury-induced mechanical hypersensitivity requires C-low threshold mechanoreceptors
It is reported that a small subset of cells in the DRG expresses the low abundance vesicular glutamate transporter VGLUT3 (also known as SLC17A8), which impairs mechanical pain sensation and the mechanical hypersensitivity to normally innocuous stimuli that accompanies inflammation, nerve injury and trauma.