Abstract:
:Capsaicin, the main pungent ingredient in "hot" chili peppers, elicits buming pain by activating specific (vanilloid) receptors on sensory nerve endings. The cloned vanilloid receptor (VR1) is a cation channel that is also activated by noxious heat. Here, analysis of heat-evoked single channel currents in excised membrane patches suggests that heat gates VR1 directly. We also show that protons decrease the temperature threshold for VR1 activation such that even moderately acidic conditions (pH < or = 5.9) activate VR1 at room temperature. VR1 can therefore be viewed as a molecular integrator of chemical and physical stimuli that elicit pain. Immunocytochemical analysis indicates that the receptor is located in a neurochemically heterogeneous population of small diameter primary afferent fibers. A role for VR1 in injury-induced hypersensitivity at the level of the sensory neuron is presented.
journal_name
Neuronjournal_title
Neuronauthors
Tominaga M,Caterina MJ,Malmberg AB,Rosen TA,Gilbert H,Skinner K,Raumann BE,Basbaum AI,Julius Ddoi
10.1016/s0896-6273(00)80564-4subject
Has Abstractpub_date
1998-09-01 00:00:00pages
531-43issue
3eissn
0896-6273issn
1097-4199pii
S0896-6273(00)80564-4journal_volume
21pub_type
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