The nasal cavity accommodates peripheral chemoreceptors for the olfactory, vomeronasal and trigeminal system. In mammals, part of the common chemical sense is made up by free endings of the trigeminal nerve which are distributed throughout the nasal cavity and respond to a variety of substances. The most potent stimulus of nasal trigeminal chemoreceptors nicotine is sensed by nicotinic acetylcholine receptors (nAChR) that are expressed in trigeminal sensory neurons. In the present study, the effects of (-)menthol on nAChR agonist responses were examined. Whole-cell recordings from acutely isolated rat trigeminal neurons (P20 ±3d) reviled that the nicotinic receptor agonists acetylcholine, (±)epibatidine and (-) nicotine induced robust currents in a dose dependent manner with IC50 values of 72 mM, 36 nM, 38 mM, respectively. It has been shown that (-)menthol induces a sensation of cold mediated by the cold receptor TRPM8. Bath application of menthol (10-750mM) at 25°C induced reversible inward currents between 20 and 300 pA in 62% of the cells (n=61). In the presence of menthol currents induced by 75 mM nicotine were significantly reduced in amplitude. Inhibition of the nicotinic response by menthol was independent of the current induced by menthol itself. The IC50 value for inhibition by (-)menthol was 112 mM. These findings suggest that menthol may have an effect on the nAChR that is independent of cold receptor activation.