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The vanilloid receptor-1 (VR1) is a ligand-gated, non-selective cation
channel expressed predominantly by sensory neurons. VR1 responds to noxious
stimuli including capsaicin, the pungent component of chilli peppers, heat
and extracellular acidification, and it is able to integrate simultaneous
exposure to these stimuli. These findings and research linking
capsaicin with nociceptive behaviours (that is, responses to painful stimuli
in animals have led to VR1 being considered as important for
pain sensation. Here we have disrupted the mouse VR1 gene using standard gene
targeting techniques. Small diameter dorsal root ganglion neurons isolated
from VR1-null mice lacked many of the capsaicin-, acid- and heat-gated responses
that have been previously well characterized in small diameter dorsal root
ganglion neurons from various species. Furthermore, although the VR1-null
mice appeared normal in a wide range of behavioural tests, including responses
to acute noxious thermal stimuli, their ability to develop carrageenan-induced
thermal hyperalgesia was completely absent. We conclude that VR1 is required
for inflammatory sensitization to noxious thermal stimuli but also that alternative
mechanisms are sufficient for normal sensation of noxious heat.