2012/01/25 by M. Hans, Michael Hans, M. Wilhelm +3
Biochemistry, Genetics and Molecular Biology · Neuroscience · #Ion Channels and Receptors #Ion channel regulation and function #Nicotinic Acetylcholine Receptors Study
paper · pdf · doi:10.1093/chemse/bjr128
openalex publication_date 2012/01/25 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/25
In this study, we have investigated how the function of native and recombinant nicotinic acetylcholine receptors (nAChRs) is modulated by the monoterpenoid alcohol from peppermint (-) menthol. In trigeminal neurons (TG), we found that nicotine (75 μM)-activated whole-cell currents through nAChRs were reversibly reduced by menthol in a concentration-dependent manner with an IC₅₀ of 111 μM. To analyze the mechanism underlying menthol's action in more detail, we used single channel and whole-cell recordings from recombinant human α4β2 nAChR expressed in HEK tsA201 cells. Here, we found a shortening of channel open time and a prolongation of channel closed time, and an increase in single channel amplitude leading in summary to a reduction in single channel current. Furthermore, menthol did not affect nicotine's EC₅₀ value for currents through recombinant human α4β2 nAChRs but caused a significant reduction in nicotine's efficacy. Taken together, these findings indicate that menthol is a negative allosteric modulator of nAChRs.