Low-threshold Heat Response Antagonized by Capsazepine in Chick Sensory Neurons, which are Capsaicin Insensitive.

ANTONIA MARIN BURGIN; ANDREAS KLUSCH; STEPHAN REPPENHAGEN; MARLEN PETERSEN

New Orleans

Congreso; Meeting of the society for neuroscience; 2000

Society for Neuroscience

The heat-transducing receptor VR1 cloned from rat sensory neurons can be activated by noxious heat and capsaicin (CAP). As the response of sensory neurons to CAP is species dependent, it is conceivable that responses to noxious heat and CAP could be transduced by distinct receptors across different species. We investigated responses to noxious heat from a CAP insensitive (chick) and a CAP sensitive (rat) species. In chick, whole-cell patch-clamp experiments in isolated DRG neurons revealed two populations of neurons with thresholds to heat activated at ~43°C or ~53°C. In cobalt uptake experiments, the proportion of neurons showing a heat-induced response increased from 10.2% ± 2.1 at 39°C to 27.0% ± 2.1 at 46°C. Rat neurons yielded comparable results in heat experiments. Surprisingly, the competitive CAP receptor antagonist capsazepine effectively blocked heat-induced responses in both species, verified by patch-clamp and cobalt uptake methods. Ruthenium red reduced the proportion of heat-responsive neurons almost completely in both species with cobalt uptake method. We conclude that chick DRG neurons express a low-threshold heat-transducing receptor with a pharmacological profile distinct from the low-threshold heat receptor VR1. The data support the idea that there might be heat receptor subtypes with differences in the CAP binding site.