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Impaired nociception and pain sensation in mice lacking the capsaicin receptor.
TLDR
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. Expand
Cellular and Molecular Mechanisms of Pain
TLDR
Genetic, electrophysiological, and pharmacological studies are elucidating the molecular mechanisms that underlie detection, coding, and modulation of noxious stimuli that generate pain. Expand
TRPA1 Mediates the Inflammatory Actions of Environmental Irritants and Proalgesic Agents
TLDR
Using TRPA1-deficient mice, it is shown that this channel is the sole target through which mustard oil and garlic activate primary afferent nociceptors to produce inflammatory pain. Expand
The Cloned Capsaicin Receptor Integrates Multiple Pain-Producing Stimuli
TLDR
It is shown that protons decrease the temperature threshold for VR1 activation such that even moderately acidic conditions (pH < or = 5.9) activate VR1 at room temperature, and VR1 can be viewed as a molecular integrator of chemical and physical stimuli that elicit pain. Expand
Bradykinin and nerve growth factor release the capsaicin receptor from PtdIns(4,5)P2-mediated inhibition
TLDR
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. Expand
Molecular mechanisms of nociception
TLDR
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. Expand
The menthol receptor TRPM8 is the principal detector of environmental cold
TLDR
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. Expand
Distinct subsets of unmyelinated primary sensory fibers mediate behavioral responses to noxious thermal and mechanical stimuli
TLDR
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. Expand
Injury-induced mechanical hypersensitivity requires C-low threshold mechanoreceptors
TLDR
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. Expand
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