Differential responses to odorant analogs after recovery from nerve transection.

We previously found that exposure-induced increase in odor sensitivity involves, at least in part, the olfactory epithelium. We did this by exposing mice to 5 alpha-androst-16-en-3-one (androstenone) and measuring changes in the epithelium. Past research showed that sensitivity to androstenone also could be induced by exposing individuals to 4-(4',4'-dimethylcyclohexyl)-2-methylcyclohexanone (DMCMC), a structural and functional analog of androstenone. What remained unknown is whether structural and/or functional odorant analogs share peripheral components. In the current work, we used a well-established model to disconnect the olfactory epithelium from the olfactory bulbs (BNX) to disrupt mechanisms underlying olfactory coding (when the afferents reinnervate the bulb, they do not synapse in their original glomeruli), and to examine the effects of disruption and restoration on exposure-induced odor sensitivity. In this study, we determined whether analogs of androstenone, viz., 5 alpha-androstan-3-one (androstanone) and DMCMC, could induce sensitivity to androstenone after BNX. Results demonstrate that exposure to either androstanone or DMCMC can induce sensitivity to androstenone in control mice. Different results were observed in mice that had recovered from bilateral BNX. Exposure to androstanone for 10 days immediately after surgery increased sensitivity to androstenone; however, exposure to DMCMC did not. These results suggest that androstanone and DMCMC, although apparent perceptual analogs of androstenone, may be using different pathways of olfaction within the central nervous system (CNS).