Ngf-independent upregulation of low threshold heat response in capsaicin-insensitive sensory neurons.

ANTONIA MARIN BURGIN; ANDREAS KLUSCH; JULIA WACH; S. ENGERT; MARLEN PETERSEN

San Diego

Congreso; Meeting of the society for neuroscience; 2001

Society for Neuroscience

The heat transducing receptor VR1 in mammalian sensory neurons is regulated by NGF. Here, we describe a heat response in chick and rat DRG neurons under conditions without NGF. Dissociated neurons were stimulated with heat (44°C)and responsive neurons were detected by cobalt uptake method. To determine the NGF dependence of heat response, two approaches were used: (i) Neurons were kept under culture conditions with or without NGF in the medium for one to three days; (ii) neurons were pre-injured by a tight ligation of the sciatic nerve for up to six days and were kept in culture for one day without NGF. With time in culture, in medium without NGF the change in the proportion of chick neurons responding to 44°C was converse to that of rat neurons. While in chick the proportion of positive neurons increased from 2% at day one to 23% at day three, the proportion of responsive rat neurons decreased from 43% to 13%. Under culture conditions with NGF, in rat, the proportion of positive neurons did not change significantly with time, while in chick there was an increase similar to that observed in experiments without NGF. The upregulation of heat response in chick seen under culture conditions was also observed after injury of the sciatic nerve. In patch-clamp experiments, a subpopulation of rat neurons responded to heat but not to capsaicin after time in culture without NGF. Our results support the idea of a heat receptor which is upregulated under pathopysiological conditions independently of NGF, in contrast to the VR1. The proposed receptor might be involved in thermal hyperalgesia after nerve injury.