In order to investigate the consequences of postnatal odorant exposure on a specific population of olfactory sensory neurons (OSNs), we have taken the following experimental approach. MOR23-GFP mice were daily exposed to Lyral for 21 days starting at birth and three lines of investigations were carried out. Using anatomical analysis we observe that the density of OSNs expressing MOR23 decreases after odorant exposure. This decrease concerns primarily matures OSN (MOR23-OMP+). In order to study molecular changes within individual OSNs, mRNA levels for olfactory signaling pathway components were quantitatively analyzed using qPCR on GFP-labeled neurons (7 per mouse). mRNAs for CNGA2, PDE1C and MOR23 olfactory receptor were up-regulated in exposed mice, whereas ACIII transcript levels remained stable. This effect is not permanent: we observed an anatomical and a molecular recovery. Patch-clamp recordings on MOR23 dendritic knobs correlate with qPCR datas. To exclude any aspecific effect due to a possible Lyral toxicity we performed EOG, immunohistochemistry and qPCR on total olfactory epithelium (OE). These experiments show that 3 weeks of Lyral exposure does not damage the OE. Then qPCR on isolated cells reveals that the effect is couple ligand-receptor dependant: M71 neurons are not affected by acetophenone exposure. Finally, we performed behavioral experiments on mice from both groups. Exposed mice favored their exposure odor in olfactory preference test and spend more time exploring Lyral than non-exposed mice. These observations suggest that the environment can induce plasticity in olfactory sensory neurons
