The detection of painful stimuli occurs primarily at the peripheral terminals of specialized sensory neurons called nociceptors. These small--diameter neurons transmit this information to the central nervous system, ultimately eliciting a perception of pain or discomfort. The capsaicin (vanilloid) receptor, an excitatory ion channel expressed at nociceptors, plays an important role in transducing thermal and inflammatory pain. Mice lacking the VR1 gene have deficits in thermal- or inflammation-induced hyperalgesia, which confirms the involvement of this channel in pain sensation, especially the sensation of heat-evoked pain.