The impact of nicotine on the olfactory memory and its relationship with TRPA1.

Olfactory disorders are related to cognitive decline, yet effective treatments remain limited. Cigarette smoke impairs olfaction, but one of its components, nicotine, can protect nerve cells in the central nervous system. Transient receptor potential ankyrin 1 (TRPA1) is expressed in central olfactory tract conduction and can be activated by nicotine. We therefore investigated whether nicotine influences olfaction through TRPA1. After inducing olfactory damage with methimazole, one of the following agents was then administered for 42 days to wild-type (WT) and TRPA1 knockout (TRPA1 KO) mice: phosphate-buffered saline, cigarette smoke extract, or nicotine. Olfactory behavioral testing and histological analyses were performed. In WT mice, intraoral nicotine improved olfactory memory and reduced neuronal apoptosis in the piriform cortex (PC). In TRPA1 KO mice, however, these effects of nicotine were abolished. Nicotine improved olfaction through TRPA1 in central olfactory tract conduction. Nicotine may thus represent a potential therapeutic strategy for olfactory impairment.