Open AccessJournal Article
Capsaicin: cellular targets, mechanisms of action, and selectivity for thin sensory neurons.
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This article is published in Pharmacological Reviews.The article was published on 1991-06-01 and is currently open access. It has received 1812 citations till now. The article focuses on the topics: Capsazepine.read more
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The capsaicin receptor: a heat-activated ion channel in the pain pathway
Michael J. Caterina,Mark Schumacher,Makoto Tominaga,Tobias A. Rosen,Jon D. Levine,David Julius +5 more
TL;DR: 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.
Journal ArticleDOI
Impaired Nociception and Pain Sensation in Mice Lacking the Capsaicin Receptor
Michael J. Caterina,A. Leffler,Annika B. Malmberg,William J. Martin,Jodie A. Trafton,K. R. Petersen-Zeitz,Martin Koltzenburg,Allan I. Basbaum,David Julius +8 more
TL;DR: 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.
Journal Article
Animal Models of Nociception
TL;DR: It is concluded that although the neural basis of the most used tests is poorly understood, their use will be more profitable if pain is considered within, rather than apart from, the body's homeostatic mechanisms.
Journal Article
Vanilloid (Capsaicin) Receptors and Mechanisms
Arpad Szallasi,Peter M. Blumberg +1 more
TL;DR: This paper focuses on hot pepper, which is eaten on a daily basis by an estimated one-quarter of the world’s population and has potential to be a biological target for regenerative medicine.
Journal ArticleDOI
The Vanilloid Receptor: A Molecular Gateway to the Pain Pathway
Michael J. Caterina,David Julius +1 more
TL;DR: The analysis of vanilloid receptor gene knockout mice confirms the involvement of this channel in pain sensation, as well as in hypersensitivity to noxious stimuli following tissue injury, and demonstrates the existence of redundant mechanisms for the sensation of heat-evoked pain.