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Biomedical subjects

Karen K Yee

Publications and source records attributed to Karen K Yee.

3 recordsLinked to original sources

Characterization and long-term maintenance of rat taste cells in culture.

Taste cells have a limited life span and are replaced from a basal cell population, although the specific factors involved in this process are not well known. Short- and long-term cultures of other sensory cells have facilitated efforts to understand the signals involved in proliferation, differentiation, and senescence, yet few studies have reported successful primary culture protocols for taste cells. Furthermore, no studies have demonstrated both proliferation and differentiation in vitro. In this study, we have developed an in vitro culture system to maintain and utilize rat primary taste cells for more than 2 months without losing key molecular and biochemical features. Gustducin, phospholipase C-beta2 (PLC-beta2), T1R3, and T2R5 mRNA were detected in the cultured cells by reverse transcriptase-polymerase chain reaction. Western blot analysis demonstrated gustducin and PLC-beta2 expression in the same samples, which was confirmed by immunocytochemistry. Labeling with bromo-2-deoxyuridine (BrdU) demonstrated proliferation, and a subset of BrdU-labeled cells were also immunoreactive for either gustducin or PLC-beta2, indicating differentiation of newly generated cells in vitro. Cultured cells also exhibited increases in intracellular calcium in response to several taste stimuli. These results indicate that taste cells from adult rats can be generated and maintained under the described conditions for at least 2 months. This system will enable further studies of the processes involved in proliferation, differentiation, and function of mammalian taste receptor cells in an in vitro preparation.

Animals↗

Transduction and coding.

Odor transduction and quality coding involves a cascade of events that occur at the level of the olfactory epithelium and olfactory bulbs. Odorants bind to one or a few specific olfactory receptors located in the cilia of olfactory neurons. These olfactory receptor proteins make up the largest gene family discovered and are diverse between and within species. The change of chemical signals to neural signals in the olfactory neurons involves G-coupled proteins and the cascade of second messenger pathways that open ion channels to depolarize the cell and trigger a series of action potentials carried along the receptor cell axon resulting in release of glutamate at synapses with mitral cells within the olfactory bulb. These neural signals in the olfactory bulb produce unique odor maps that play an important role in our ability to detect and discriminate thousands of different odorants. The olfactory neurons are replaced throughout life from a population of slowly dividing basal cells within the epithelium. Disease, infection, injury or aging can interfere with neuronal cell replacement as well as transduction and coding processes, resulting in impairment and distortions of olfactory performance.

Aging↗

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).

Androstenes↗