Meeting Abstract
The stress response in vertebrates is intimately associated with appetitive behavior. Not only are there changes in food preference and consumption rates following acute or chronic application of stressors, but modulation of the peripheral sensory environment is also a direct outcome of HPA axis activation. Glucocorticoids (GCs) are the principal stress hormones that affect sensory tissues by interaction with glucocorticoid receptors (GRs). We have found that GRs are expressed in the mouse taste bud, specifically in sweet- and umami-sensitive cells that express a subunit of the sweet receptor, T1r3. Further, when mice are restrained (2h), GR translocates to the nucleus. Concomitant with these changes, we have observed increased expression of chaperone molecules (Hsp70 and Hsp90) in stressed taste buds from mice, and these proteins are known to be directly involved in GC-based signaling in target tissues. Lastly, we have recently found that GR colocalizes with lamin-B in the nuclear envelope which may temper taste receptor cell responsiveness to free GCs. While the link between sweet taste and stress have been thoroughly studied in human and rodent models, our work is the first to examine how GCs can directly activate the network of stress-responsive genes in the taste epithelium.
