Author: Wegner S, University of Marburg, Department of Physiology and Pathophysiology.
Names and affiliation of other authors:
Wollweber BT, Schneider H, Voigt H, Braun HA.
University of Marburg, Department of Physiology and Pathophysiology
Oral or poster: Poster
It is well known that menthol is stimulating and sensitising cold receptor transduction. The underlying ionic mechanisms, however, are still under debate. Blockade of Ca-currents with reduction of Ca-dependent K-currents have been discussed. Recordings from DRG neurons, however, clearly demonstrated Menthol induced activation of TRPM8 (CMR1) ion channels. Moreover, more recent studies suggest multiple actions of menthol including, for example, excitation of TRPV3 and inhibition of TRPA1 (ANKTM1) channels.
In our present study, menthol was used as an agent to examine (de-)sensitisation effects in the brain. The experiments have been done on hypothalamic GT1-7 neurons. These neurons, as we could demonstrate with PCR studies, do not express the TRPM8. Moreover, our patch-clamp studies demonstrated a pronounced reduction of an outward current which cannot be explained by the conventional assumptions about the action of menthol via TRP channels. Our data rather point to an inhibition of potassium channels.
Experiments are in progress, in combination with a computer model which includes the potentially relevant currents, to evaluate the specific site of menthol action and its consequences for the neuronal dynamics.