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The capsaicin receptor in nociceptive neurons is a target for the sensitizing actions of algogenic inflammatory mediators. Capsaicin and potential endogenous ligands are thought not to gate this heat-activated ion channel but to sensitize it so profoundly that even room temperature can open it. We investigated the temperature dependency of capsaicin-induced CGRP release from nociceptive nerve fibers in isolated rat skin over a range of ambient temperatures using different agonist concentrations (10 -7 -10 -5 M) and KCl (60 mM) for control. Ambient temperature (4-40 o C) showed no significant influence on the basal iCGRP outflow. The supramaximal capsaicin concentration of 10 -6 M as a stimulus evoked a response that was not significantly diminished by temperatures decreasing from 40 to 24 o C but lost 65% of its amplitude between 24 and 14 o C (Q 10 ~6.7). Such a collapse of the response occurred between 40 and 32 o C at lower capsaicin concentration (10 -7 M). The concentration-response curves showed a rightward shift upon cooling from 40 to 24 o C and a major loss of slope and maximum effect at 14 o C which formally describes a noncompetitive antagonism. KCl-induced iCGRP release showed a much more linear temperature dependency (Q 10 ~2.4 between 24 and 14 o C). Significant capsaicin responses even at 8 o C suggest a contribution of noxious-cold sensitive neurons known to coexpress CGRP and the capsaicin receptor. The heat-activated ion channels (TRPV1-4) are thought to play a significant role in inflammatory pain which is effectively relieved by cooling. The present results contribute to understanding this phenomenon.