Protons potentiate low threshold heat response in capsaicin-insensitive chick sensory neurons.

ANTONIA MARIN BURGIN; ANDREAS KLUSCH; A.SCHMALFUSS; MARLEN PETERSEN

San Diego

Congreso; Meeting of the society for neuroscience; 2001

Society for Neuroscience

Sensory neurons from chick respond to low threshold heat but not to capsaicin. Therefore, we propose a heat receptor distinct from the cloned VR1. Recent experiments suggest that the upregulation of heat responsive neurons in chick with time in culture is independent of NGF, in contrast to the VR1 in mammals. Heat and capsaicin responses via VR1 are both sensitized by acidification. Here, we asked whether the heat response of the putative receptor is also sensitized by protons. Experiments were performed on dissociated DRG neurons from chick. Under whole-cell voltageclamp conditions the effect of low pH of the bath solution on heat evoked inward currents was investigated. In a subpopulation of neurons inward currents were elicited by heat stimuli in the noxious temperature (48 to 52 °C) range. With repeated stimuli, the amplitude of the heat-evoked current was unchanged. Acidification of the bath solution from the control pH of 7.3 to a pH of 5.8 enhanced the heat-evoked current by a mean of 50 % in a reversible manner. Repeated co-application of heat and protons resulted in a small decrease in amplitude. Although these neurons do not respond to capsaicin alone, the heat response was augmented by co-application of heat and capsaicin in a reversible manner. These results suggest that protons and capsaicin potentiate the heat-evoked response of the receptor transducing noxious heat in chick sensory neurons. It is conceivable that the putative receptor is involved in neuropatic pain in mammals.