Capsaicin, the main pungent ingredient in 'hot' chilli peppers, elicits a sensation of burning pain by selectively activating sensory neurons that convey information about noxious stimuli to the central nervous system We have used an expression cloning strategy based on calcium influx to isolate a functional cDNA encoding a capsaicin receptor from sensory neurons This receptor is a non-selective cation channel that is structurally related to members of the TRP family of ion channels The cloned capsaicin receptor is also activated by increases in temperature in the noxious range, suggesting that it functions as a transducer of painful thermal stimuli in vivo

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The capsaicin receptor: a heat-activated ion channel in the pain pathway

We describe those sensations that are unpleasant, intense, or distressing as painful. Pain is not homogeneous, however, and comprises three categories: physiological, inflammatory, and neuropathic pain. Multiple mechanisms contribute, each of which is subject to or an expression of neural plasticity-the capacity of neurons to change their function, chemical profile, or structure. Here, we develop a conceptual framework for the contribution of plasticity in primary sensory and dorsal horn neurons to the pathogenesis of pain, identifying distinct forms of plasticity, which we term activation, modulation, and modification, that by increasing gain, elicit pain hypersensitivity.

https://science.sciencemag.org/content/sci/288/5472/1765.full.pdf

Neuronal plasticity: increasing the gain in pain.

https://www.cell.com/cell/pdf/S0092-8674(09)01243-4.pdf

Cellular and Molecular Mechanisms of Pain

The capsaicin (vanilloid) receptor VR1 is a cation channel expressed by primary sensory neurons of the "pain" pathway. Heterologously expressed VR1 can be activated by vanilloid compounds, protons, or heat (>43 degrees C), but whether this channel contributes to chemical or thermal sensitivity in vivo is not known. Here, we demonstrate that sensory neurons from mice lacking VR1 are severely deficient in their responses to each of these noxious stimuli. VR1-/- mice showed normal responses to noxious mechanical stimuli but exhibited no vanilloid-evoked pain behavior, were impaired in the detection of painful heat, and showed little thermal hypersensitivity in the setting of inflammation. Thus, VR1 is essential for selective modalities of pain sensation and for tissue injury-induced thermal hyperalgesia.

http://science.sciencemag.org/content/sci/288/5464/306.full.pdf

Impaired Nociception and Pain Sensation in Mice Lacking the Capsaicin Receptor

http://www.columbia.edu/cu/biology/courses/w3004/recitation7.pdf

Peter W. Reeh

Papers

PL13 Saying NO to H2S

cAMP/PKA Signaling Pathway in Vagal Sensory Neurons: Role of 2 Enhanced by PGE Transient Evoked by Chemical Stimulation Is

painisometric contraction and their relation to Kinin peptides in human trapezius muscle during

Cardiac Sympathetic Afferents in Cats Myocardial Ischemia Recruits Mechanically Insensitive

Current in Embryonic Rat Sensory Neurons Prostaglandins Suppress an Outward Potassium