Impaired nociception and pain sensation in mice lacking the capsaicin receptor.

By M. Caterina, A. Leffler, Annika B. Malmberg, W. Martin, J. Trafton, K. R. Petersen-Zeitz, M. Koltzenburg, A. Basbaum, D. Julius. Science, 2000

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Cellular and Molecular Mechanisms of Pain (2009, positive): “Lack of such sensitization in TRPV1-deficient mice provides genetic support for the idea that TRPV1 is a key component of the mechanism through which inflammation produces thermal hyperalgesia (Caterina et al., 2000; Davis et al., 2000).”
Sensory neuron-specific GPCR Mrgprs are itch receptors mediating chloroquine-induced pruritus. (2009, neutral): “Radiant heat (Hargreaves) test was performed as previously described (Caterina et al., 2000).”
An introduction to TRP channels. (2006, background): “TRPV1-null mice lack vanilloid sensitivity in nociceptive, inflammatory, and thermoregulatory assays; a crucial role for TRPV1 in thermal hyperalgesia is evident (79, 80).”
TRP Channels (2012, neutral): “In particular, it was widely assumed that TRPV2 would be responsible for (part of) the residual heat sensitivity of Trpv1 knockout mice (52).”
The TRP Superfamily of Cation Channels (2005, background): “Nevertheless, the knockout mice exhibited a clear and pronounced deficit in thermal hyperalgesia resulting from prior inflammation (107, 108).”
TRP channels and pain. (2013, background): “…promotes a transient hypothermia associated with heat loss through cutaneous vasodilation, sweating, and perhaps other afferent-evoked thermoregulatory actions (part of the attraction of eating hot peppers in hot climates) (Caterina et al. 2000, Issekutz et al. 1950, Jancsó-Gábor et al. 1970).”