Abstracts - Association for Chemoreception Sciences
Abstracts - Association for Chemoreception Sciences
Abstracts - Association for Chemoreception Sciences
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#P199 POSTER SESSION IV:<br />
CHEMICAL SIGNALING AND BEHAVIOR;<br />
ANIMAL BEHAVIOR/PSYCHOPHYSICS;<br />
CHEMOSENSATION AND METABOLISM;<br />
VOMERONSASAL AND CHEMICAL<br />
COMMUNICATION<br />
#P200 POSTER SESSION IV:<br />
CHEMICAL SIGNALING AND BEHAVIOR;<br />
ANIMAL BEHAVIOR/PSYCHOPHYSICS;<br />
CHEMOSENSATION AND METABOLISM;<br />
VOMERONSASAL AND CHEMICAL<br />
COMMUNICATION<br />
Palatability of Cycloheximide or Caffeine Mixed with<br />
Sugar in Hamsters<br />
Elizabeth M. Casey, Bradley K. Formaker, Thomas P. Hettinger,<br />
Marion E. Frank<br />
University of CT Health Center Farmington, CT, USA<br />
Multiple coding mechanisms <strong>for</strong> bitter stimuli are suggested<br />
by taste receptive-field specificity, quality and palatability.<br />
Quality and palatability of quinine (Qui), salicin (Sal), caffeine<br />
(Caf) and cycloheximide (Cyc) differ in hamsters (Mesocricetus<br />
auratus). Quality, studied with generalizations of conditioned<br />
taste aversions (CTA), differs <strong>for</strong> each; but, each stimulus is<br />
aversive measured in preference to water. Hamster taste aversions<br />
are generally reduced by adding sucrose. Thus, aversions<br />
to 1mM Qui, 10mM Sal, 30mM Caf and 30µM Cyc were<br />
compared to the 4 stimuli mixed with 500mM sucrose. Qui<br />
and Sal palatability increased with sucrose added but Caf and<br />
Cyc did not (Lloyd et al. 2012). To determine concentrationdependence,<br />
5, 10 and 30mM Caf and 5, 10 and 30mM Cyc<br />
(with and without 500mM sucrose) were tested <strong>for</strong> 2-bottle<br />
48-hr preference vs. water (R-L bottle positions reversed daily).<br />
Each hamster randomly received 14 stimuli based on a modified<br />
Latin Square. A preference ratio [ml stimulus ingested/ml total<br />
fluid ingested; indifference = 0.5] was computed and differences<br />
tested with analysis of variance (a =0.05). Hamsters strongly<br />
preferred sucrose over water [0.725]. Caf and Cyc aversions were<br />
unaffected by concentration or the addition of sucrose. Average<br />
preference ratios collapsed across concentration were 0.210 <strong>for</strong><br />
Caf and 0.225 <strong>for</strong> Caf + sucrose; 0.164 <strong>for</strong> Cyc and 0.151 <strong>for</strong><br />
Cyc + sucrose. Reducing bitter stimulus concentration did not<br />
increase amelioration by sucrose. This is consistent with Cyc<br />
aversions (1-hr tests) quickly developing, even to Cyc-sucrose<br />
mixtures without affecting sucrose intake (Hettinger et al. 2007),<br />
and Cyc serving as a CTA UCS when injected IP (Formaker<br />
et al. 2009). Acknowledgements: Supported by UConn SDM<br />
Alumni Research Fellowship and NIH grant DC004099.<br />
Regulation of Taste Responses by TNF<br />
Jinghua Chai, Pu Feng, Hong Wang<br />
Monell Chemical Senses Center Philadelphia, PA, USA<br />
Patients with inflammatory diseases often experience taste<br />
alterations. Yet, how inflammation affects taste function is<br />
not fully understood. Previously, we showed that tumor<br />
necrosis factor (TNF), a potent proinflammatory cytokine,<br />
is preferentially expressed in a subset of type II taste cells.<br />
The level of TNF in taste cells can be further induced by<br />
inflammatory stimuli such as lipopolysaccharide (LPS), a<br />
bacterial cell-wall component that elicits acute inflammation.<br />
Although TNF plays important roles in mediating inflammation<br />
and cell death in various tissues, its roles in taste buds remain<br />
to be determined. In this study, we carried out taste behavioral<br />
tests and gene expression analyses in wild-type and TNFdeficient<br />
mice. Lickometer tests were conducted to examine<br />
behavioral responses to salty, sour, bitter, sweet, and umami taste<br />
compounds be<strong>for</strong>e and after LPS-induced inflammation. Our<br />
results showed that TNF-deficient mice were less sensitive to<br />
the bitter compound quinine be<strong>for</strong>e any treatments. After LPS<br />
injection, wild-type mice displayed a range of altered responses<br />
to the taste compounds, especially to the sweet taste compound<br />
sucrose. In contrast, TNF-deficient mice did not show a<br />
significant alteration in response to sucrose after LPS treatment,<br />
suggesting that TNF plays an important role in regulating<br />
taste response to sucrose under LPS-induced inflammation.<br />
Furthermore, gene expression analyses by quantitative RT-PCR<br />
showed that the levels of several inflammation- and cell-deathrelated<br />
genes were increased by LPS in wild-type mice, but<br />
were not induced in TNF-deficient mice. Together, these results<br />
suggest that TNF may be an important mediator <strong>for</strong> taste<br />
dysfunction associated with inflammation. Acknowledgements:<br />
This study was supported by NIH/NIDCD grants DC010012<br />
and DC011735.<br />
POSTER PRESENTATIONS<br />
<strong>Abstracts</strong> are printed as submitted by the author(s).<br />
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