149 Slide <strong>Chemosensory</strong> Coding and ClinicalANALYSES OF HUMAN AXILLARY ODORS AND THEIRPRECURSORS IN NORMAL AND STRESSFUL SITUATIONSYabuki M. 1 , Takeuchi K. 1 , Hagura T. 1 , Hasegawa Y. 1 1 Tokyo ResearchLaboratory, Kao Corporation, Tokyo, JapanOur laboratory previously reported the 3-Hydroxy-3-methylhexanoicacid (3H3MH) and 3-methyl-3-sulfanylhexan-1-ol (3M3SH) as keyodorants in human axillary sweat (Hasegawa, 2004). We had alsoelucidated the occurrence of cysteine-linked precursor of 3M3SH on theaxillary skin and applied for a patent for the use of body odor indicator(Yabuki, 2004). One objective of this study is to analyze amino acidlinked axillary odor precursors quantitatively. A second objective is toevaluate the effect of mentally stressful situation on axillary odor. Inthis study, we evaluated axillary odor of healthy American women (n =26, aged 18-63) and collected their sweat samples in both normal (day1) and mentally stressful situation (day 2). During 10-minute stresssession trained moderator asked math, trivia and word questions tosubjects continuously. LC-MS/MS analyses showed there wascorrelation between the precursor levels on skin surface and odorintensity. Whereas the ratios of glutamine-linked two odor precursors,Gln-3H3MH to Gln-3M2H (3-Methyl-2-Hexenoic acid) wereapproximately 7:1 with no inter-subject variation, the ratios of Gln-3H3MH to Cys-3M3SH were unique to subjects. This finding indicatesa presence of common synthetic pathway for the glutamine-linked3H3MH and 3M2H. The temperature and other circumstances remainedunchanged for testing two days. However, 70% of subjects of the day 2had higher odor and precursor levels compared to day 1. Some subjectshad more than three times higher amounts of precursors. This resultsuggests mental stress induced perspiration acts as an accelerator forstrong odor formation.150 Poster <strong>Chemosensory</strong> Coding and ClinicalVOLATILE CONSTITUENTS OF HUMAN SKIN: GENETICFACTORS AND BIOCHEMICAL INDIVIDUALITYNovotny M.V. 1 , Soini H.A. 1 , Klouckova I. 1 , Wiesler D. 1 , OberzaucherE. 2 , Grammer K. 2 , Dixon S. 3 , Gong F. 3 , Brereton R. 3 , Penn D. 4 1 Institutefor Pheromone Research, Indiana University, Bloomington, IN; 2Anthropology, Ludwig-Boltzmann-Institute for Urban Ethology, Vienna,Austria; 3 Centre for Chemometrics, University of Bristol, Bristol,United Kingdom; 4 Konrad Lorenz Institute for Ethology, AustrianAcademy of Sciences, Vienna, AustriaHuman skin surface contains different types of glands that excretenumerous compounds, including polar and nonpolar lipids and peptides,but also small volatile organic compounds (VOCs) which can beolfactorily active. Human body odors can reflect physiological state andmood of individuals. Body odors appear to have their genetic attributes(e.g., MHC-related odors), while resident microflora can contribute totheir occurrence. The studies of VOCs in human emanations have beenlimited by the lack of quantitative techniques for comparing a largenumber of individuals. We have recently developed a high-throughputand highly quantitative technique for VOC profiling, which allowed tomonitor precisely about 400 compounds by gas chromatography/massspectrometry. Repeatedly collected VOC samples of 195 subjects wereanalyzed. Advanced chemometric methods were employed forevaluation of the VOC profiles. Numerous marker compoundsdistinguishing gender, families and individuals were located. Variousoxygenated compounds were identified as prominent markermetabolites. Their biochemical and genetic significance will bediscussed.151 Poster <strong>Chemosensory</strong> Coding and ClinicalPROBING THE CEREBELLAR ROLE IN SNIFFING WITHTRANSCRANIAL MAGNETIC STIMULATION (TMS)Mainland J. 1 , Ivry R.B. 1 , Sobel N. 1 1 Neuroscience, University ofCalifornia, Berkeley, Berkeley, CASniffs are modulated in response to odor concentration; higherconcentrations of odor induce lesser-volume sniffs. Studies usingfunctional magnetic resonance imaging (fMRI) and lesion patients bothsuggest a cerebellar role in this olfactomotor response. However, fMRIis a correlational technique and lesion patients may have developedcompensatory strategies that differ from healthy subjects. To probewhether cerebellar function is essential to the olfactomotor response inhealthy subjects, we will use transcranial magnetic stimulation. We firstset out to determine the relevant time-window for TMS application. Wefound that sniff volume was concentration-independent for the first 150ms, but inversely proportional to odorant concentration after 160 ms(t(8) = 3.12, p < 0.014). TMS has been shown to have a temporalresolution of 50 ms in visual tasks, suggesting that single-pulse TMScan probe the time course of cerebellar involvement in the olfactomotorresponse. To probe this time-course, single-pulse TMS will be appliedto the cerebellum at 100 ms preceding the start of the sniff, the start ofthe sniff, 100 ms after the start of the sniff and 200 ms after the start ofthe sniff. Influence of the TMS pulse on both sniffing and olfactoryperformance will be assessed.152 Slide Taste Chemoreception"FATTY"—A PRIMARY TASTEChalé-Rush A. 1 , Mattes R.D. 1 1 Foods and Nutrition, Purdue University,West Lafayette, INPreliminary psychophysical data indicate that long-chain fatty acidsof varying saturation are effective taste stimuli. This is consistent withelectrophysiological and animal data. The present study sought toisolate the taste property of three 18-C fatty acids by masking othersensory attributes. Linoleic, oleic, and stearic fatty acids were sonicatedin deionized water in concentrations ranging from 0.00028 % to 5%(w/v). To minimize oxidation, samples were stored under nitrogen.Stimuli were prepared fresh daily and 0.01% EDTA (w/v) was added toeach sample. The contribution of viscosity was minimized by additionof 5% Acacia (w/v) to the vehicle. Lubricity effects were reduced byaddition of 5% mineral oil (w/v). To determine if the effective stimuluswas an oxidation product, oxidized linoleic acid was included amongthe test stimuli. Testing was conducted with participants wearing noseclips and under red light to eliminate olfactory and visual cues.Detection thresholds were obtained using a three-alternative, forcedchoiceascending concentration presentation procedure. The criterionstopping rule was three consecutive correct identifications of a targetsample. Incorrect identification resulted with presentation of the nexthigher fatty acid concentration. The mean detection threshold forlinoleic was 0.11% (SD = 0.24), for oleic 0.02% (SD = 0.04), for stearic0.09% (SD = 0.21) and oxidized linoleic 0.05% (SD = 0.11). Theresults are indicative of a gustatory component to fat perception inhumans. Supported by NIH grant R01 DK45294-1438
153 Slide Taste ChemoreceptionTASTE CELLS IN THE GASTRO-INTESTINAL TRACTBezençon C. 1 , Le Coutre J. 1 , Damak S. 1 1 Nestlé Research Center,Lausanne, SwitzerlandCells that resemble taste bud cells have been described in the gastrointestinaltract and are thought to play a role in gut chemoreception. Tounderstand the role of these cells, we set out to determine which genes,and in particular which taste signal transduction elements, they express.For bitter, sweet and umami, the taste signaling cascade is initiated inthe taste receptor cells by activation of G-protein coupled receptors(T2rs for bitter, T1rs for sweet and umami). The signaling pathwaysdownstream the receptors include gustducin, a G-protein expressedselectively in taste cells, phospholipase Cβ2 (PLCβ2) and Trpm5, acalcium activated cation channel. Using immunohistochemistry and RT-PCR we found that T1r1, T1r3, α-gustducin, PLCβ2 and Trpm5 areexpressed in solitary cells disseminated throughout the villi and theglands of the mouse gastro-intestinal tract. Real time PCR showed thatT1r1, T1r3 and Trpm5 are also expressed in the human intestine. Colocalizationstudies showed a large degree of co-localization of T1r3,T1r1, α-gustducin and Trpm5 in the villi of the duodenum, whereasPLCβ2 is expressed in a different subset of cells. In the glands of theduodenum, Trpm5 rarely co-localizes with T1r3 or α-gustducin, butabout 30% of Trpm5 expressing cells also express PLCβ2. In the colonTrpm5 co-localizes with α-gustducin but very few cells express T1r3,T1r1 or PLCβ2, and these cells do not express Trpm5 or α-gustducin.Our data show that the “taste cells” in the gut are heterogeneous andsuggest that the duodenal “taste cells” may respond to L-amino acids.154 Slide Taste ChemoreceptionTHE REGULATION OF NEURAL TARGETING IN THEDEVELOPING GUSTATORY SYSTEMKrimm R.F. 1 , Lopez G.F. 1 , Patel A. 1 1 Anatomical Sciences andNeurobiology, University of Louisville Medical Center, Louisville, KYDuring development, axons of the chorda tympani nerve mustnavigate to specific locations, the fungiform papillae, in the lingualepithelium. We quantified the accuracy with which gustatory fibersinnervate fungiform papillae from embryonic day 14.5-18.5. By E14.5chorda tympani fibers penetrate the epithelium of most fungiformpapillae forming a “neural bud”. Initial targeting was incrediblyaccurate: specifically, 94% of the fungiform papillae on the tongue areinnervated at E14.5. Targeting accuracy increased from E14.5 to E18.5of development as more papillae became innervated and inappropriateinnervation was withdrawn. We have determined that one factorregulating the accuracy of initial neural targeting in the taste system isthe neurotrophin, brain-derived neurotrophic factor (BDNF). BDNF isproduced by developing gustatory epithelia. In mice lacking BDNF, thechorda tympani branches extensively below the epithelium at E14.5 andE16.5, but does not penetrate the epithelium forming a neural bud. Thisincreased branching occurs even though BDNF knockout mice arelosing geniculate neurons between E14.5 and E16.5. A few neural budsfinally form at E17.5, 3 days after they are present in wild type mice. Inmice overexpressing BDNF in non-gustatory epithelium, chordatympani fibers are misdirected to inappropriate locations. Thesetargeting effects are specific to BDNF and do not occur with otherneurotrophins (NT3 and NT4). Taken together these findingsdemonstrate that initial targeting of chorda tympani fibers is extremelyaccurate and that this accuracy is regulated by BDNF. Supported byNIDCD grant DC07176 to RFK.155 Slide Taste ChemoreceptionSEARCHING FOR GENES AFFECTING PREFERENCES FORSWEET FOODS; A FINNISH FAMILY STUDYKeskitalo K. 1 , Knaapila A. 1 , Kallela M. 2 , Palotie A. 1 , Wessman M. 1 ,Peltonen L. 3 , Tuorila H. 1 , Perola M. 3 1 University of Helsinki, Helsinki,Finland; 2 Helsinki University Central Hospital, Helsinki, Finland;3 National Public Health Institute, Helsinki, Finland135 members (31 % male, 69 % female, 19 to 78 years old) of 24Finnish families, genome-scanned with 360 microsatellite markers,were phenotyped for chemosensory traits (intensity of PROP by filterpaper method, intensity and pleasantness of 3, 7.5, and 18.75 % sucrosesolutions) and for use and pleasantness of sweet foods (questionnaire).Intensities were rated using the labeled magnitude scale (LMS) andpleasantness using the labeled affective magnitude scale (LAM).Phenotypes for use frequency and pleasantness (7-point scales) of sweetfoods were constructed as means of ratings given to 5 items (chocolate,candies, ice cream, sweet pastry, sweet desserts). Program MERLINwas used for variance component linkage analysis of these quantitativetraits. Heritabilities for PROP intensity, sweetness intensity andpleasantness of 18.75 % sucrose solution, and use frequency andpleasantness of sweet foods were 65, 3, 48, 54 and 46 %, respectively.The highest LOD score of 4.28, located on Chr16p11.2 was obtained foruse frequency of sweet foods, suggesting that this locus harborsvariation(s) influencing this trait. Funded by the Academy of Finland(206327).156 Slide Taste ChemoreceptionMOLECULAR MECHANISMS OF HUMAN SWEET WATERTASTEBufe B. 1 , Winnig M. 1 , Galindo-Cuspinera V. 2 , Breslin P. 2 , MeyerhofW. 1 1 Molecular Genetics, German Institute of Human NutritionPotsdam-Rehbruecke, Nuthetal, Germany; 2 Monell Chemical SensesCenter, Philadelphia, PASweet water taste is elicited by chemicals such as the sweet allostericinhibitor lactisole that only tastes sweet when rinsed from the mouthwith water. Similarly, saccharin, which has only a negligible sweetnessat high concentrations, tastes intensely sweet during water rinses.Intriguingly, these effects were mimicked in calcium imagingexperiments of HEK293T G16Gust44 cells expressing the human sweetreceptor. Saccharin activated these cells at low sweet-tastingconcentrations (EC50 of ~0.1 mM), but at higher concentrationsattenuated the response (IC50 ~50 mM) suggesting the presence of alow affinity inhibitory allosteric site. This effect was reversible sincesaccharin washout elicited robust signals. This suggests that the sweetwater taste of saccharin is caused by the release from inhibition of theallosteric site, which activates the receptor. While lactisole applicationon sweet receptor expressing cells does not cause any receptoractivation, rinsing away lactisole does. Further analysis revealed thatcells expressing the sweet receptor have elevated basal calcium levelsrelative to mock transfected cells that are reduced by the application oflactisole. Therefore, lactisole may act as an inverse agonist by shiftingthe constitutively active sweet receptor into the inactive form. Thesignals upon lactisole removal may be explained by a rebound of thereceptor to its constitutively active form. Thus, sweet water-taste inhumans can be elicited by the release of the constitutively active sweetreceptor during the wash out of an allosteric inhibitor.39
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