The olfactory mucosa (OM) is the primary site of odorant detection, and its axonal projections relay information to brain structures for signal processing. We have previously observed that olfactory function… Click to show full abstract
The olfactory mucosa (OM) is the primary site of odorant detection, and its axonal projections relay information to brain structures for signal processing. We have previously observed that olfactory function can be affected during a prolonged stress challenge in Wistar rats. The stress response is a neuroendocrine retro‐controlled loop allowing pleiotropic adaptive tissue alterations, which are partly mediated through the release of glucocorticoid hormones. We hypothesised that, as part of their wide‐ranging pleiotropic effects, glucocorticoids might affect the first step of olfactory detection. To study this, we used a number of approaches ranging from the molecular detection and functional characterisation of glucocorticoid receptors (GRs) in OM cells, to the study of GR acute activation in vivo at the molecular, electrophysiological and behavioural levels. In contrast to previous reports, where GR was reported to be exclusive in olfactory sensory neurones, we located functional GR expression mostly in olfactory ensheathing cells. Dexamethasone (2 mg/kg) was injected intraperitoneally to activate GR in vivo, and this led to functional odorant electrophysiological response (electro‐olfactogram) and OM gene expression changes. In a habituation/cross‐habituation test of olfactory sensitivity, we observed that DEX‐treated rats exhibited higher responsiveness to a complex odorant mixture. These findings support the idea that olfactory perception is altered in stressed animals, as glucocorticoids might enhance odour detection, starting at the first step of detection.
               
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